Ludvig Magne Sollid

• Hjort, Rebecka; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Jonkers, Iris & Lundin, Knut [Vis alle 10 forfattere av denne artikkelen] (2026). Human Leukocyte Antigen-DQ Allotypes in Adults Screened for Celiac Disease Reveal Historical Misdiagnosis - Results From the Trøndelag Health Study. Clinical Gastroenterology and Hepatology. ISSN 1542-3565. doi: 10.1016/j.cgh.2026.07.033. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2026). One mechanism, two diseases: Involvement of enzyme–substrate complexes in the pathogenesis of celiac disease and rheumatoid arthritis. Proceedings of the National Academy of Sciences of the United States of America (PNAS). ISSN 0027-8424. 123(37). doi: 10.1073/pnas.2600933123. Fulltekst i vitenarkiv
• Lindeman, Ida; Officer, Aengus; Dahal-Koirala, Shiva; Risnes, Louise Fremgaard; Hjort, Rebecka & Lundin, Knut [Vis alle 9 forfattere av denne artikkelen] (2026). A predisposing effect of HLA class II genes in celiac disease by skewing the naive CD4⁺T cell receptor repertoire. Proceedings of the National Academy of Sciences of the United States of America (PNAS). ISSN 0027-8424. 123(26). doi: 10.1073/pnas.2520636123. Fulltekst i vitenarkiv
• Heggelund, Julie Elisabeth; Ahmad, Ahmad Ali; Johannesen, Marie Kongshaug; Sekulic, Nikolina & Sollid, Ludvig Magne (2026). Cryo-EM structure of the complex between transglutaminase 2 and the 45 kDa domain of fibronectin. Journal of Biological Chemistry. ISSN 0021-9258. 302(9), s. 1–11. doi: 10.1016/j.jbc.2026.113326. Fulltekst i vitenarkiv
• Bjørnevik, Kjetil Lauvland; Mahler, João Vitor; Bilodeau, Philippe A.; Rød, Brit Ellen; Romanow, Gabriela & Mikami, Takahisa [Vis alle 19 forfattere av denne artikkelen] (2026). CD4⁺ T cells reactive to Epstein-Barr virus late lytic antigens are enriched in individuals with multiple sclerosis. Science Translational Medicine. ISSN 1946-6234. 18(858). doi: 10.1126/scitranslmed.adz6566.
• Vaz, Filipa Baltazar da Costa; Lindeman, Ida; Hoffmann, Henriette H.; Skagen, Christine; Steffensen, Anne Katrine & Bjørnholt, Jørgen Vildershøj [Vis alle 10 forfattere av denne artikkelen] (2026). Distinct systemic and gut IgA responses to bacteria of the human upper gastrointestinal tract. Cell reports. 45(8), s. 1–21. doi: 10.1016/j.celrep.2026.117721. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Hjort, Rebecka; Jonkers, Iris H.; Withoff, Sebo; Hveem, Kristian & Lundin, Knut [Vis alle 8 forfattere av denne artikkelen] (2026). A model for predicting celiac disease among undiagnosed subjects established with data from the HUNT4 study. BMC Gastroenterology. 26(1). doi: 10.1186/s12876-026-04837-y. Fulltekst i vitenarkiv
• Officer, Aengus; Watson, Corey T.; Engelbrecht, Eric; Dahal-Koirala, Shiva; Risnes, Louise Fremgaard & Lundin, Knut [Vis alle 9 forfattere av denne artikkelen] (2026). Immunoglobulin gene polymorphisms shape the naïve B-cell receptor repertoire; relevance to celiac disease. Genes and Immunity. ISSN 1466-4879. 27, s. 210–222. doi: 10.1038/s41435-026-00384-4. Fulltekst i vitenarkiv
• Risnes, Louise Fremgaard; Brottveit, Margit; Robertsen, Ida; Ibsen, Jostein Holen; Aabakken, Lars & Johannesen, Marie Kongshaug [Vis alle 12 forfattere av denne artikkelen] (2025). Research Communication: Teriflunomide Does Not Affect Gluten-Specific T-Cell Activity in Coeliac Disease—A Randomised, Placebo-Controlled Trial. Alimentary Pharmacology and Therapeutics. ISSN 0269-2813. 62(10), s. 1027–1031. doi: 10.1111/apt.70301. Fulltekst i vitenarkiv Vis sammendrag

  Coeliac disease is an autoimmune disorder driven by gluten and managed through a strict gluten-free diet. We tested teriflunomide, a drug known for its ability to alter T-cell activity, in a phase 2a trial of 15 patients with coeliac disease. Participants received teriflunomide or placebo including a loading dose, followed by a 3-day oral gluten challenge to monitor T-cell responses. The main aim was to observe attenuation of gluten-specific T-cell activation markers after gluten exposure. We found no significant differences in T-cell activity between groups, concluding that teriflunomide is ineffective as a non-dietary treatment for coeliac disease

• Al-Toma, Abdulbaqi; Zingone, Fabiana; Branchi, Federica; Schiepatti, Annalisa; Malamut, Georgia & Canova, Cristina [Vis alle 21 forfattere av denne artikkelen] (2025). European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach. United European Gastroenterology Journal (UEG Journal). ISSN 2050-6406. 13(10), s. 1855–1886. doi: 10.1002/ueg2.70119. Fulltekst i vitenarkiv Vis sammendrag

  Introduction Since the publication of the first European Society for the Study of Coeliac Disease (ESsCD) guidelines in 2019, significant advancements have emerged in the diagnosis of coeliac disease (CeD) in adults. These 2025 guidelines incorporate new evidence to refine diagnostic strategies, aiming for improved accuracy of testing, and enhance overall quality of clinical care. Methods A multidisciplinary panel of experts revised the ESsCD guidelines using the AGREE II instrument (Appraisal of Guidelines for Research and Evaluation II) and the GRADE methodology (The Grading of Recommendations Assessment, Development, and Evaluation). Clinical questions were structured using the PICO format, and statements and recommendations were finalised through a Delphi consensus process. Literature quality was assessed using AMSTAR-2 and QUADAS-2 tools. Results The updated guidelines are presented in two parts. Part 1 focuses on adult CeD diagnosis, introducing major changes such as a conditional no-biopsy approach for selected adults with high-titre IgA anti-TG2 serology (≥ 10 × ULN). Regarding serology, the use of validated high-performance ELISAs displaying a high diagnostic accuracy is emphasised, while routine use of IgA anti-Endomysium serology is no longer recommended for confirmation. Revised duodenal biopsy protocols now mandate at least four samples from the second part of the duodenum, with bulb biopsies conditionally included. The guidelines provide structured approaches for diagnosing potential CeD, seronegative villous atrophy, and CeD in individuals already on a gluten-free diet. HLA-DQ2/DQ8 typing is recommended for diagnostic clarification in select cases. Conclusions The updated 2025 ESsCD guidelines provide a comprehensive framework for the diagnosis of CeD in adults. By integrating evolving diagnostic strategies, minimising over-testing, and patient-centred care approaches, they aim to optimise patient outcomes, quality of life and use of diagnostic resources at the same time.

• Stamnæs, Jorunn; Stray, Daniel; Pré, Marie Fleur du; Risnes, Louise Fremgaard; Dewan, Alisa & Shaik, Jakeer [Vis alle 9 forfattere av denne artikkelen] (2025). IFN-gamma is a direct driver of crypt hyperplasia in celiac disease. Journal of Clinical Investigation. ISSN 0021-9738. 135(20). doi: 10.1172/JCI194858. Fulltekst i vitenarkiv Vis sammendrag

  Crypt hyperplasia is a key feature of celiac disease (CeD) and several other small intestinal inflammatory conditions. Analysis of the gut epithelial crypt zone by mass spectrometry–based tissue proteomics revealed a strong IFN-γ signal in active CeD. This signal, hallmarked by increased expression of MHC molecules, was paralleled by diminished expression of proteins associated with fatty acid metabolism. Crypt hyperplasia and the same proteomic changes were observed in WT mice administered IFN-γ. In mice with conditional KO of the IFN-γ receptor in gut epithelial cells, these signature morphological and proteomic changes were not induced with IFN-γ administration. IFN-γ was thus a driver of crypt hyperplasia in CeD by acting directly on crypt epithelial cells. The results are relevant to other enteropathies with involvement of IFN-γ.

• Alam, Mohammad Sayeef; Wolford, Brooke N.; Hveem, Kristian; Lundin, Knut; Withoff, Sebo & Jonkers, Iris H. [Vis alle 9 forfattere av denne artikkelen] (2025). Genetic differences between diagnosed and undiagnosed Celiac disease: a population-based study. Human Genetics. ISSN 0340-6717. 144, s. 1071–1078. doi: 10.1007/s00439-025-02778-2. Fulltekst i vitenarkiv Vis sammendrag

  A large proportion of individuals with celiac disease (CeD) remain undiagnosed, often presenting at an older age of onset or with non-classical symptoms compared to diagnosed cases. Such heterogeneity might be related to genetic factors. The aim was to utilize a CeD-screened adult population to compare the genetic variants in known and newly diagnosed cases. In the fourth wave of the population-based Trøndelag Health Study (HUNT4) 826 CeD and 51,516 non-CeD individuals were included. Medical registries identified 361 previously diagnosed cases, while screening identified 465 new cases. A validated polygenic risk score (PRS) was used to assess the genetic risk of CeD among the two case groups versus non-CeD individuals. Additional genetic variants not included in the PRS were also analyzed. The PRS distinguished cases from non-cases with high accuracy (AUROC: 85% for known cases, 83% for new cases). The genetic variation explained by the PRS was similar for known and new cases (17.1% versus 14.5%). The odds ratio for being in the highest genetic risk group (top 10%) was 22.7 (95% CI 14.1–36.4) for known cases and 18.6 (95% CI 12.4–27.9) for new cases versus the median group (40%-60%). Differences in effect size among specific genome-wide variants were observed but were not significantly associated with CeD. A validated PRS showed significant genetic difference between CeD cases and the general population, with similar association in both known and newly diagnosed cases. This suggests that genetic architectures of the two groups are comparable, implying that other non-genetic factors may drive CeD in adults.

• Pré, Marie Fleur du; Kleppa, Liv; Dewan, Alisa; Meling, Maureen Tania; Høydahl, Lene Støkken & Besser, Harrison A. [Vis alle 8 forfattere av denne artikkelen] (2025). Peyer’s Patch B Cells Sample Transglutaminase-Gluten Complexes and Drive Celiac Disease Autoimmunity. Gastroenterology. ISSN 0016-5085. doi: 10.1053/j.gastro.2025.06.021. Fulltekst i vitenarkiv Vis sammendrag

  Background & aims: The production of autoantibodies against the enzyme transglutaminase 2 (TG2) in celiac disease likely results from TG2-specific B cells receiving help from gluten-specific CD4+ T cells in gut-associated lymphoid tissues (GALT) via the formation of transient enzyme-substrate complexes formed between TG2 and gluten. Where in the body enzymatically active TG2 encounters gluten peptides remains unknown. Methods: A model to study the celiac disease-relevant T-cell-B-cell interactions in GALT has been developed. Mice expressing HLA-DQ2.5 received TG2-specific B cells and gluten-specific T cells by adoptive transfer and were subsequently orally immunized with a model antigen containing the the B-cell and T-cell epitopes. Results: Orally immunized HLA-DQ2.5 knockin mice developed TG2-specific gut immunoglobulin (Ig)A and serum IgG responses. Activated TG2-specific B cells were present in Peyer's patches and in gut-draining mesenteric lymph nodes, resembling what is seen in human celiac disease. We demonstrate that TG2-specific B cells in Peyer's patches sample TG2 when the protein is perfused into the gut lumen. Conclusion: The model supports a mechanism in which TG2-gluten complexes formed in the gut lumen are taken up by TG2-specific B cells in GALT. We propose that this pathway plays an important role in driving the anti-TG2 IgA autoantibody response in patients with celiac disease. The model provides a platform to explore novel approaches for celiac disease therapies.

• Løberg, Runa Ingrunsdotter; Dewan, Alisa; Kleppa, Liv; Pré, Fleur du & Sollid, Ludvig Magne (2025). A Mouse Model for Generation of Gut Lamina Propria Plasma Cells Specific for a Deamidated Gluten Peptide. European Journal of Immunology. ISSN 0014-2980. 55(3). doi: 10.1002/eji.202451658. Fulltekst i vitenarkiv
• Porret, Raphaël; Alcaraz-Serna, Ana; Peter, Benjamin; Bernier-Latmani, Jeremiah; Cecchin, Rebecca & Alfageme-Abello, Oscar [Vis alle 22 forfattere av denne artikkelen] (2025). T cell receptor precision editing of regulatory T cells for celiac disease. Science Translational Medicine. ISSN 1946-6234. 17(790). doi: 10.1126/scitranslmed.adr8941. Fulltekst i vitenarkiv
• Iversen, Rasmus; Heggelund, Julie Elisabeth; Das, Saykat; Høydahl, Lene Støkken & Sollid, Ludvig Magne (2025). Enzyme-activating B-cell receptors boost antigen presentation to pathogenic T cells in gluten-sensitive autoimmunity. Nature Communications. 16. doi: 10.1038/s41467-025-57564-5. Fulltekst i vitenarkiv Vis sammendrag

  Autoantibodies against the enzyme transglutaminase 3 (TG3) are characteristic to the gluten-sensitive skin disorder dermatitis herpetiformis (DH), which is an extraintestinal manifestation of celiac disease. We here demonstrate that TG3-specific B cells can activate gluten-specific CD4+ T cells through B-cell receptor (BCR)-mediated internalization of TG3-gluten enzyme-substrate complexes. Stereotypic anti-TG3 antibodies using IGHV2-5/IGKV4-1 gene segments enhance the catalytic activity of TG3, and this effect translates into increased gluten presentation to T cells when such antibodies are expressed as BCRs. The crystal structure of TG3 bound to an IGHV2-5/IGKV4-1 Fab shows that antibody binding to a β-sheet in the catalytic core domain causes the enzyme to adopt the active conformation. This mechanism explains the production of stereotypic anti-TG3 autoantibodies in DH and highlights a role for TG3-specific B cells as antigen-presenting cells for gluten-specific T cells. Similar boosting effects of autoreactive BCRs could be relevant for other autoimmune diseases, including rheumatoid arthritis.

• Alam, Mohammad Sayeef; Thomas, Laurent Francois; Brumpton, Ben Michael; Hveem, Kristian; Lundin, Knut & Withoff, Sebo [Vis alle 10 forfattere av denne artikkelen] (2025). Population screening of adults identifies novel genetic variants associated with celiac disease. Scientific Reports. 15(1). doi: 10.1038/s41598-025-04421-6. Fulltekst i vitenarkiv Vis sammendrag

  Celiac disease (CeD) is an autoimmune disease driven by a complex genetic interplay within and beyond the human leukocyte antigen (HLA) region. Despite this, half of its heritability remains unexplained, with most of the unidentified variants located in non-protein coding regions. Here we performed a genome-wide association study among 52,342 adults screened for CeD, including 465 previously undiagnosed and 361 already diagnosed cases, which mitigated the likely disease misclassification present in previous studies. Genotyping and imputation yielded approximately 24.9 million variants for analysis. The study identified 15 novel associations (P < 5E-08) in 12 loci in addition to all the previously associated loci at lower significance thresholds (P < 5E-03). The 5p15.33 locus in the long non-coding RNA gene (LINC01019) showed the highest potential for a true association with CeD. Notably, variants in 5p15.33 has also been associated with rheumatoid arthritis, suggesting a new shared autoimmune locus.

• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf; Warren, David John; Bolstad, Nils & Mjønes, Patricia Gjertrud [Vis alle 11 forfattere av denne artikkelen] (2025). The Prevalence and Rate of Undiagnosed Celiac Disease in an Adult General Population, the Trøndelag Health Study, Norway. Clinical Gastroenterology and Hepatology. ISSN 1542-3565. 23(7), s. 1143–1151. doi: 10.1016/j.cgh.2024.06.027. Fulltekst i vitenarkiv Vis sammendrag

  Background & Aims This study aimed to determine the total prevalence of celiac disease (CeD), including undiagnosed cases, in a population-based study of adults screened for CeD. Methods The study used the fourth Trøndelag Health Study (HUNT4), conducted in 2017–2019, where 56,042 adult (aged >20 years) residents of Nord-Trøndelag County, Norway, participated. Serum samples from 54,505 participants were analyzed for anti-transglutaminase 2 IgA and IgG. Seropositive individuals were invited for a clinical assessment, including upper endoscopy with duodenal biopsies. Previously diagnosed and seronegative CeD cases were identified through linkage to hospital records and the Norwegian Patient Registry. Results The rate of CeD seropositivity was 2.0% (1107/54,505). Out of these, 724 individuals attended the clinical assessment. Additionally, the hospital records and registry identified individuals with a known CeD diagnosis, that were seronegative or without serology in HUNT4 or seropositive in HUNT4 but did not participate in the clinical assessment. In total, the study confirmed a new CeD diagnosis after participation in HUNT4 in 470 individuals and a known CeD diagnosis before participation in HUNT4 in 383 individuals. The total biopsy-confirmed prevalence of CeD was 1.5% (853/56,042), and the ratio of new, previously undiagnosed CeD cases (after HUNT4) to known, previously diagnosed CeD cases (before HUNT4) was 1.2:1 (470/383). Conclusions The total prevalence of CeD in this population-based study of adults in Norway was high and many individuals were previously undiagnosed. Detection of CeD should be improved, because early diagnosis is crucial for effective management and prevention of complications.

• Andersen, Ina Lervåg; Lukina, Polina; Dyrli, Ole Thomas; Klaasen, Rolf; Warren, David & Bolstad, Nils [Vis alle 12 forfattere av denne artikkelen] (2025). Serological screening for coeliac disease in an adult general population: the HUNT study. Gut. ISSN 0017-5749. 74(6), s. 918–925. doi: 10.1136/gutjnl-2024-333886. Fulltekst i vitenarkiv Vis sammendrag

  Background A large proportion of individuals with coeliac disease (CeD) remain undiagnosed. Objective The aim of this study was to assess serological screening for CeD in the adult general population. Design The study was based on the fourth Trøndelag Health Study, a population-based study performed 2017–2019 in Nord-Trøndelag County, Norway, including 56 042 participants >20 years of age (54% participation rate). Serum samples were analysed with a dual antitransglutaminase 2 (TG2) IgA and IgG assay and seropositive participants were invited to endoscopy with duodenal biopsies. A CeD diagnosis was given if mucosal damage (Marsh grade 3) was found. Results Histological evaluation of 657 seropositive participants confirmed CeD in 423. The positive predictive value (PPV) of a positive TG2 IgA was 73.3% (95% CI 69.7% to 77.0%) for biopsy-confirmed CeD. TG2 IgA ≥10 times the upper limit of normal (ULN), as used in the no-biopsy approach in children, increased the PPV to 88.1% (95% CI 84.8% to 91.4%). Primary TG2 IgG response was found in 87 participants, five of whom had biopsy-confirmed CeD. One of the participants with CeD primarily responding with TG2 IgG was IgA deficient. The PPV of a positive TG2 IgG was 5.8% (95% CI 1.9% to 12.9%) and of TG2 IgG ≥10× ULN was 9.5% (95% CI 1.2% to 30.4%) for biopsy-confirmed CeD in TG2 IgA-negative individuals. Conclusion The TG2 IgA assay showed excellent abilities as a screening tool for CeD in the adult general population. However, the diagnostic accuracy of TG2 IgG was too poor for selectively identifying individuals with CeD.

• Johansen, Anette; Sandve, Geir Kjetil Ferkingstad; Maxwell, Joseph R.; Smithson, Glennda; Sollid, Ludvig Magne & Stamnæs, Jorunn (2024). Biopsy Proteome Score Performs Well as an Effect Measure in a Gluten Challenge Trial of Celiac Disease. Clinical Gastroenterology and Hepatology. ISSN 1542-3565. 23(5), s. 758–765.e8. doi: 10.1016/j.cgh.2024.08.005. Fulltekst i vitenarkiv Vis sammendrag

  Background and Aims Development of novel treatments for celiac disease is dependent on precise tools to monitor changes in gluten-induced mucosal damage. Current histology measures are subjective and difficult to standardize. Biopsy proteome scoring is an objective alternative to histology which is based on robust changes in biological pathways that directly reflect gluten-induced mucosal damage. In this study, we aimed to evaluate biopsy proteome scoring as an effect measure in a clinical trial setting by measuring intestinal remodeling in response to oral gluten challenge. Methods We analyzed biopsies from a 14-day gluten challenge trial of treated celiac disease patients that consumed 3 g (n = 6) or 10 g (n = 7) gluten per day. Sections from individually embedded biopsies collected before and after challenge were processed for proteome scoring (n = 109) and measurement of villus height-to-crypt depth ratio (n = 58). Proteome scores were compared with histology, intraepithelial lymphocyte frequency and plasma interleukin-2. Results Change in proteome scores were significant for the group of patients who consumed 10 g gluten, but not for the group who consumed 3 g gluten. Altogether, 8 of 13 patients had changes in delta proteome scores above the cutoff. Proteome scores correlated with villus height-to-crypt depth ratios both at run-in and at day 15. Proteome scores at day 15 correlated with intraepithelial lymphocyte frequency and with plasma interleukin-2 levels measured 4 hours post–gluten intake. Conclusion Biopsy proteome scoring is a simple and reliable measure of gluten-induced mucosal remodeling in response to 14-day oral gluten challenge. ClinicalTrials.gov, Number: NCT03409796.

• Risnes, Louise Fremgaard; Reims, Henrik Mikael; Doyle, Ronan Mathieu; Qiao, Shuo-Wang; Sollid, Ludvig Magne & Lundin, Knut [Vis alle 7 forfattere av denne artikkelen] (2024). Gluten-Free Diet Induces Rapid Changes in Phenotype and Survival Properties of Gluten-Specific T Cells in Celiac Disease. Gastroenterology. ISSN 0016-5085. 167(2), s. 250–263. doi: 10.1053/j.gastro.2024.03.027. Fulltekst i vitenarkiv Vis sammendrag

  Background & Aims The treatment of celiac disease (CeD) with gluten-free diet (GFD) normalizes gut inflammation and disease-specific antibodies. CeD patients have HLA-restricted, gluten-specific T cells persisting in the blood and gut even after decades of GFD, which are reactivated and disease driving upon gluten exposure. Our aim was to examine the transition of activated gluten-specific T cells into a pool of persisting memory T cells concurrent with normalization of clinically relevant biomarkers during the first year of treatment. Methods We followed 17 CeD patients during their initial GFD year, leading to disease remission. We assessed activation and frequency of gluten-specific CD4+ blood and gut T cells with HLA-DQ2.5:gluten tetramers and flow cytometry, disease-specific serology, histology, and symptom scores. We assessed gluten-specific blood T cells within the first 3 weeks of GFD in 6 patients and serology in an additional 9 patients. Results Gluten-specific CD4+ T cells peaked in blood at day 14 while up-regulating Bcl-2 and down-regulating Ki-67 and then decreased in frequency within 10 weeks of GFD. CD38, ICOS, HLA-DR, and Ki-67 decreased in gluten-specific cells within 3 days. PD-1, CD39, and OX40 expression persisted even after 12 months. IgA–transglutaminase 2 decreased significantly within 4 weeks. Conclusions GFD induces rapid changes in the phenotype and number of gluten-specific CD4+ blood T cells, including a peak of nonproliferating, nonapoptotic cells at day 14. Subsequent alterations in T-cell phenotype associate with the quiescent but chronic nature of treated CeD. The rapid changes affecting gluten-specific T cells and disease-specific antibodies offer opportunities for clinical trials aiming at developing nondietary treatments for patients with newly diagnosed CeD.

• Pavlović, Milena; Hajj, Ghadi al; Kanduri, Chakravarthi; Pensar, Johan; Wood, Mollie Elizabeth & Sollid, Ludvig Magne [Vis alle 8 forfattere av denne artikkelen] (2024). Improving generalization of machine learning-identified biomarkers using causal modelling with examples from immune receptor diagnostics. Nature Machine Intelligence. 6(1), s. 15–24. doi: 10.1038/s42256-023-00781-8. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Tolerance-inducing therapies in coeliac disease — mechanisms, progress and future directions. Nature reviews: Gastroenterology & hepatology. ISSN 1759-5045. 21(5), s. 335–347. doi: 10.1038/s41575-024-00895-3. Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Eggen, Petter Tinbod; Mjønes, Patricia Gjertrud; Rønne, Elin & Bolstad, Nils [Vis alle 18 forfattere av denne artikkelen] (2024). Coeliac disease in the Trøndelag Health Study (HUNT), Norway, a population-based cohort of coeliac disease patients. BMJ Open. 14:e077131(1), s. 1–7. doi: 10.1136/bmjopen-2023-077131. Fulltekst i vitenarkiv Vis sammendrag

  Purpose - Coeliac disease (CD) is a common disorder and affects about 1% of the population worldwide. CD in the Trøndelag Health Study (HUNT) is a population-based cohort study which was established to provide new knowledge about CD that can improve the diagnostics and management, prevent the onset or progression and expand the knowledge about the role of genetics of the disease. Participants - The cohort is based on the fourth wave of the population-based HUNT study (HUNT4), Norway, performed during 2017–2019, also including linkage to hospital records and the Norwegian Patient Registry (NPR). A total of 54 541 HUNT4 participants with available sera were screened for CD by serology. All seropositive participants were invited to a clinical assessment, including endoscopy with duodenal biopsies, during 2019–2023. Findings to date - A total of 1107 HUNT4 participants (2%) were seropositive for CD and 1048 were eligible for clinical assessment, including biopsy. Of these, 724 participants attended the clinical assessment and 482 were identified with CD. In addition, 371 participants with CD were identified through the hospital records and NPR. In total, 853 participants in HUNT4 with biopsy-verified CD diagnosis were identified. Future plans - All participants in the study will be invited to a follow-up assessment after at least 1 year, including repeated standard serological testing, endoscopy and tissue sampling. The collected data and material will be used to establish the true population-based prevalence of CD. The consequences of CD, including symptoms, deficiencies and comorbidity, will be investigated and possible triggers and predictors, will be studied. With access to serum samples from the previous HUNT surveys in HUNT Biobank, serological signs of CD in prediagnostic samples of seropositive individuals will be used. Genetic studies will identify new CD markers, assess genotype–phenotype links and explore gene–environment correlations.

• Johansen, Anette; Sandve, Geir Kjetil Ferkingstad; Ibsen, Jostein Holen; Lundin, Knut; Sollid, Ludvig Magne & Stamnæs, Jorunn (2024). Biopsy Proteome Scoring to Determine Mucosal Remodeling in Celiac Disease. Gastroenterology. ISSN 0016-5085. 167(3), s. 493–504. doi: 10.1053/j.gastro.2024.03.006. Fulltekst i vitenarkiv Vis sammendrag

  Background & Aims Histologic evaluation of gut biopsies is a cornerstone for diagnosis and management of celiac disease (CeD). Despite its wide use, the method depends on proper biopsy orientation, and it suffers from interobserver variability. Biopsy proteome measurement reporting on the tissue state can be obtained by mass spectrometry analysis of formalin-fixed paraffin-embedded tissue. Here we aimed to transform biopsy proteome data into numerical scores that give observer-independent measures of mucosal remodeling in CeD. Methods A pipeline using glass-mounted formalin-fixed paraffin-embedded sections for mass spectrometry-based proteome analysis was established. Proteome data were converted to numerical scores using 2 complementary approaches: a rank-based enrichment score and a score based on machine learning using logistic regression. The 2 scoring approaches were compared with each other and with histology analyzing 18 patients with CeD with biopsies collected before and after treatment with a gluten-free diet as well as biopsies from patients with CeD with varying degree of remission (n = 22). Biopsies from individuals without CeD (n = 32) were also analyzed. Results The method yielded reliable proteome scoring of both unstained and H&E-stained glass-mounted sections. The scores of the 2 approaches were highly correlated, reflecting that both approaches pick up proteome changes in the same biological pathways. The proteome scores correlated with villus height-to-crypt depth ratio. Thus, the method is able to score biopsies with poor orientation. Conclusions Biopsy proteome scores give reliable observer and orientation-independent measures of mucosal remodeling in CeD. The proteomic method can readily be implemented by nonexpert laboratories in parallel to histology assessment and easily scaled for clinical trial settings.

• Santos, António J. M.; Unen, Vincent van; Lin, Zhongqi; Chirieleison, Steven M.; Ha, Nhi & Batish, Arpit [Vis alle 31 forfattere av denne artikkelen] (2024). A human autoimmune organoid model reveals IL-7 function in coeliac disease. Nature. ISSN 0028-0836. 632(8024), s. 401–410. doi: 10.1038/s41586-024-07716-2. Fulltekst i vitenarkiv
• Pré, Marie Fleur du; Iversen, Rasmus & Sollid, Ludvig Magne (2024). Coeliac disease: the paradox of diagnosing a food hypersensitivity disorder with autoantibodies. Gut. ISSN 0017-5749. 73(5), s. 844–853. doi: 10.1136/gutjnl-2023-331595. Fulltekst i vitenarkiv
• Lindeman, Ida; Høydahl, Lene Støkken; Christophersen, Asbjørn Otto; Risnes, Louise Fremgaard; Jahnsen, Jørgen & Lundin, Knut [Vis alle 8 forfattere av denne artikkelen] (2024). Generation of circulating autoreactive pre-plasma cells fueled by naive B cells in celiac disease. Cell reports. 43:114045(4), s. 1–23. doi: 10.1016/j.celrep.2024.114045. Fulltekst i vitenarkiv Vis sammendrag

  Autoantibodies against the enzyme transglutaminase 2 (TG2) are characteristic of celiac disease (CeD), and TG2-specific immunoglobulin (Ig) A plasma cells are abundant in gut biopsies of patients. Here, we describe the corresponding population of autoreactive B cells in blood. Circulating TG2-specific IgA cells are present in untreated patients on a gluten-containing diet but not in controls. They are clonally related to TG2-specific small intestinal plasma cells, and they express gut-homing molecules, indicating that they are plasma cell precursors. Unlike other IgA-switched cells, the TG2-specific cells are negative for CD27, placing them in the double-negative (IgD−CD27−) category. They have a plasmablast or activated memory B cell phenotype, and they harbor fewer variable region mutations than other IgA cells. Based on their similarity to naive B cells, we propose that autoreactive IgA cells in CeD are generated mainly through chronic recruitment of naive B cells via an extrafollicular response involving gluten-specific CD4+ T cells.

• Iversen, Rasmus & Sollid, Ludvig Magne (2024). Dissecting autoimmune encephalitis through the lens of intrathecal B cells. Proceedings of the National Academy of Sciences of the United States of America (PNAS). ISSN 0027-8424. doi: 10.1073/pnas.2401337121. Fulltekst i vitenarkiv
• Abadie, Valérie; Han, Arnold S.; Jabri, Bana & Sollid, Ludvig Magne (2024). New Insights on Genes, Gluten, and Immunopathogenesis of Celiac Disease. Gastroenterology. ISSN 0016-5085. 167(1), s. 4–22. doi: 10.1053/j.gastro.2024.03.042. Fulltekst i vitenarkiv
• Das, Saykat; Stamnæs, Jorunn; Høydahl, Lene Støkken; Skagen, Christine; Lundin, Knut & Jahnsen, Jørgen [Vis alle 8 forfattere av denne artikkelen] (2024). Selective activation of naïve B cells with unique epitope specificity shapes autoantibody formation in celiac disease. Journal of Autoimmunity. ISSN 0896-8411. 146, s. 1–10. doi: 10.1016/j.jaut.2024.103241. Fulltekst i vitenarkiv Vis sammendrag

  Many antibody responses induced by infection, vaccination or autoimmunity show signs of convergence across individuals with epitope-dependent selection of particular variable region gene segments and complementarity determining region 3 properties. However, not much is known about the relationship between antigen-specific effector cells and antigen-specific precursors present in the naïve B-cell repertoire. Here, we sought to address this relationship in the context of celiac disease, where there is a stereotyped autoantibody response against the enzyme transglutaminase 2 (TG2). By generating TG2-specific monoclonal antibodies from both duodenal plasma cells and circulating naïve B cells, we demonstrate a discord between the naïve TG2-specific repertoire and the cells that are selected for autoantibody production. Hence, the naïve repertoire does not fully reflect the epitope preference and gene usage observed for memory B cells and plasma cells. Instead, distinct naïve B cells that target particular TG2 epitopes appear to be selectively activated at the expense of TG2-binding B cells targeting other epitopes.

• Cubero-Leon, Elena; Madsen, Charlotte B.; Scherf, Katharina A.; Colgrave, Michelle L.; Nørgaard, Jørgen V. & Anthoni, Minna [Vis alle 9 forfattere av denne artikkelen] (2024). Barley based gluten free beer – A blessing or an uncontrollable risk? Food and Chemical Toxicology (FCT). ISSN 0278-6915. 193:115019, s. 1–9. doi: 10.1016/j.fct.2024.115019. Fulltekst i vitenarkiv Vis sammendrag

  Recent reports have highlighted that beer labelled “gluten-free”, crafted with enzymatic treatments to remove gluten, may contain polypeptides that could be immunotoxic to individuals with coeliac disease. As strict adherence to a gluten-free diet is the only way to manage this condition, accurate labelling is crucial to those with coeliac disease. This paper aims to discuss the presence, levels and immunogenicity of gluten peptides found in gluten-reduced barley beers. While advances have been made in the detection and quantification of gluten peptides in beer, there are still challenges to the interpretation of gluten measurements as well as to assess whether peptides are immunotoxic in vivo. To make progress, future efforts should involve a combination of in vivo toxicity assessment of the degraded proteins, development of standardised gluten-free production strategies to minimise variability in gluten fragment presence, guidance on how to control the outcome as well as to develop appropriate reference materials and calibrators.

• Drosu, Natalia; Bjørnevik, Kjetil Lauvland; Cortese, Marianna; Levy, Michael & Sollid, Ludvig Magne (2024). Coeliac disease as a model for understanding multiple sclerosis. Nature Reviews Neurology. ISSN 1759-4758. 20(11), s. 685–690. doi: 10.1038/s41582-024-01025-y. Fulltekst i vitenarkiv
• Meling, Maureen Tania; Kleppa, Liv; Besser, Harrison; Khosla, Chaitan; Pré, Fleur du & Sollid, Ludvig Magne (2024). Enterocyte-Derived and Catalytically Active Transglutaminase 2 in the Gut Lumen of Mice: Implications for Celiac Disease. Gastroenterology. ISSN 0016-5085. doi: 10.1053/j.gastro.2024.05.029. Fulltekst i vitenarkiv
• Heggelund, Julie Elisabeth; Das, Saykat; Stamnæs, Jorunn; Iversen, Rasmus & Sollid, Ludvig Magne (2023). Autoantibody binding and unique enzyme-substrate intermediate conformation of human transglutaminase 3. Nature Communications. 14:6216 (1), s. 1–11. doi: 10.1038/s41467-023-42004-z. Fulltekst i vitenarkiv Vis sammendrag

  Abstract Transglutaminase 3 (TG3), the autoantigen of dermatitis herpetiformis (DH), is a calcium dependent enzyme that targets glutamine residues in polypeptides for either transamidation or deamidation modifications. To become catalytically active TG3 requires proteolytic cleavage between the core domain and two C-terminal β-barrels (C1C2). Here, we report four X-ray crystal structures representing inactive and active conformations of human TG3 in complex with a TG3-specific Fab fragment of a DH patient derived antibody. We demonstrate that cleaved TG3, upon binding of a substrate-mimicking inhibitor, undergoes a large conformational change as a β-sheet in the catalytic core domain moves and C1C2 detaches. The unique enzyme-substrate conformation of TG3 without C1C2 is recognized by DH autoantibodies. The findings support a model where B-cell receptors of TG3-specific B cells bind and internalize TG3-gluten enzyme-substrate complexes thereby facilitating gluten-antigen presentation, T-cell help and autoantibody production.

• Okura, Yuu; Ikawa-Teranishi, Yuri; Mizoroki, Akihiko; Takahashi, Noriyuki; Tsushima, Takashi & Irie, Machiko [Vis alle 30 forfattere av denne artikkelen] (2023). Characterizations of a neutralizing antibody broadly reactive to multiple gluten peptide:HLA-DQ2.5 complexes in the context of celiac disease. Nature Communications. 14:8502(1), s. 1–15. doi: 10.1038/s41467-023-44083-4. Fulltekst i vitenarkiv Vis sammendrag

  Abstract In human celiac disease (CeD) HLA-DQ2.5 presents gluten peptides to antigen-specific CD4 + T cells, thereby instigating immune activation and enteropathy. Targeting HLA-DQ2.5 with neutralizing antibody for treating CeD may be plausible, yet using pan-HLA-DQ antibody risks affecting systemic immunity, while targeting selected gluten peptide:HLA-DQ2.5 complex (pHLA-DQ2.5) may be insufficient. Here we generate a TCR-like, neutralizing antibody (DONQ52) that broadly recognizes more than twenty-five distinct gluten pHLA-DQ2.5 through rabbit immunization with multi-epitope gluten pHLA-DQ2.5 and multidimensional optimization. Structural analyses show that the proline-rich and glutamine-rich motif of gluten epitopes critical for pathogenesis is flexibly recognized by multiple tyrosine residues present in the antibody paratope, implicating the mechanisms for the broad reactivity. In HLA-DQ2.5 transgenic mice, DONQ52 demonstrates favorable pharmacokinetics with high subcutaneous bioavailability, and blocks immunity to gluten while not affecting systemic immunity. Our results thus provide a rationale for clinical testing of DONQ52 in CeD.

• Iversen, Rasmus & Sollid, Ludvig Magne (2023). The Immunobiology and Pathogenesis of Celiac Disease. Annual Review of Pathology. ISSN 1553-4006. 18, s. 47–70. doi: 10.1146/annurev-pathmechdis-031521-032634. Fulltekst i vitenarkiv Vis sammendrag

  Among human leukocyte antigen (HLA)-associated disorders, celiac disease has an immunopathogenesis that is particularly well understood. The condition is characterized by hypersensitivity to cereal gluten proteins, and the disease lesion is localized in the gut. Still, the diagnosis can be made by detection of highly disease-specific autoantibodies to transglutaminase 2 in the blood. We now have mechanistic insights into how the disease-predisposing HLA-DQ molecules, via presentation of posttranslationally modified gluten peptides, are connected to the generation of these autoantibodies. This review presents our current understanding of the immunobiology of this common disorder that is positioned in the border zone between food hypersensitivity and autoimmunity.

• Chlubnova, Marketa; Christophersen, Asbjørn Otto; Sandve, Geir Kjetil Ferkingstad; Lundin, Knut Erik Aslaksen; Jahnsen, Jørgen & Dahal-Koirala, Shiva [Vis alle 7 forfattere av denne artikkelen] (2023). Identification of gluten T cell epitopes driving celiac disease. Science Advances. 9(4), s. 1–8. doi: 10.1126/sciadv.ade5800. Fulltekst i vitenarkiv Vis sammendrag

  CD4+ T cells specific for cereal gluten proteins are key players in celiac disease (CeD) pathogenesis. While several CeD-relevant gluten T cell epitopes have been identified, epitopes recognized by a substantial proportion of gluten-reactive T cells remain unknown. The identification of such CeD-driving gluten epitopes is important for the food industry and in clinical settings. Here, we have combined the knowledge of a distinct phenotype of gluten-reactive T cells and key features of known gluten epitopes for the discovery of unknown epitopes. We tested 42 wheat gluten–reactive T cell clones, isolated on the basis of their distinct phenotype and with no reactivity to known epitopes, against a panel of synthetic peptides bioinformatically identified from a wheat gluten protein database. We were able to assign reactivity to 10 T cell clones and identified a 9-nucleotide oligomer core region of five previously uncharacterized gliadin/glutenin epitopes. This work represents an advance in the effort to identify CeD-driving gluten epitopes.

• Funsten, Matthew C.; Yurkovetskiy, Leonid A.; Kuznetsov, Andrey; Reiman, Derek; Hansen, Camilla H.F. & Senter, Katharine I. [Vis alle 15 forfattere av denne artikkelen] (2023). Microbiota-dependent proteolysis of gluten subverts diet-mediated protection against type 1 diabetes. Cell Host and Microbe. ISSN 1931-3128. 31(2), s. 213–227.e9. doi: 10.1016/j.chom.2022.12.009. Fulltekst i vitenarkiv
• Das, Saykat; Stamnæs, Jorunn; Kemppainen, Esko; Hervonen, Kaisa; Lundin, Knut & Parmar, Naveen [Vis alle 12 forfattere av denne artikkelen] (2023). Separate Gut Plasma Cell Populations Produce Auto-Antibodies against Transglutaminase 2 and Transglutaminase 3 in Dermatitis Herpetiformis. Advanced Science. 10:2300401(25), s. 1–10. doi: 10.1002/advs.202300401. Fulltekst i vitenarkiv Vis sammendrag

  Abstract Dermatitis herpetiformis (DH) is an inflammatory skin disorder often considered as an extra intestinal manifestation of celiac disease (CeD). Hallmarks of CeD and DH are auto‐antibodies to transglutaminase 2 (TG2) and transglutaminase 3 (TG3), respectively. DH patients have auto‐antibodies reactive with both transglutaminase enzymes. Here it is reported that in DH both gut plasma cells and serum auto‐antibodies are specific for either TG2 or TG3 with no TG2–TG3 cross reactivity. By generating monoclonal antibodies from TG3‐specific duodenal plasma cells of DH patients, three conformational epitope groups are defined. Both TG2‐specific and TG3‐specific gut plasma cells have few immunoglobulin (Ig) mutations, and the two transglutaminase‐reactive populations show distinct selection of certain heavy and light chain V‐genes. Mass spectrometry analysis of TG3‐specific serum IgA corroborates preferential usage of IGHV2‐5 in combination with IGKV4‐1 . Collectively, these results demonstrate parallel induction of anti‐TG2 and anti‐TG3 auto‐antibody responses involving separate B‐cell populations in DH patients.

• Polak, Justyna; Wagnerberger, Johanna Henny; Torsetnes, Silje Bøen; Lindeman, Ida; Høglund, Rune Alexander Aamodt & Vartdal, Frode [Vis alle 8 forfattere av denne artikkelen] (2023). Single-cell transcriptomics combined with proteomics of intrathecal IgG reveal transcriptional heterogeneity of oligoclonal IgG-secreting cells in multiple sclerosis. Frontiers in Cellular Neuroscience. 17. doi: 10.3389/fncel.2023.1189709. Fulltekst i vitenarkiv Vis sammendrag

  The phenotypes of B lineage cells that produce oligoclonal IgG in multiple sclerosis have not been unequivocally determined. Here, we utilized single-cell RNA-seq data of intrathecal B lineage cells in combination with mass spectrometry of intrathecally synthesized IgG to identify its cellular source. We found that the intrathecally produced IgG matched a larger fraction of clonally expanded antibody-secreting cells compared to singletons. The IgG was traced back to two clonally related clusters of antibody-secreting cells, one comprising highly proliferating cells, and the other consisting of more differentiated cells expressing genes associated with immunoglobulin synthesis. These findings suggest some degree of heterogeneity among cells that produce oligoclonal IgG in multiple sclerosis.

• Amundsen, Sunniva Furre; Stamnæs, Jorunn; Lundin, Knut & Sollid, Ludvig Magne (2023). Expression of transglutaminase 2 in human gut epithelial cells: Implications for coeliac disease. PLOS ONE. 18:e0287662(6), s. 1–15. doi: 10.1371/journal.pone.0287662. Fulltekst i vitenarkiv Vis sammendrag

  Background Formation of complexes between transglutaminase 2 (TG2) and gluten can mechanistically explain why TG2 serves both as B-cell autoantigen and as an enzyme that creates deamidated gluten epitopes in coeliac disease (CeD). A model has been proposed where TG2 released from shed epithelial cells encounters high concentrations of dietary gluten peptides to form these TG2:gluten complexes. In this work we have characterised TG2 protein expression in gut epithelial cells in humans. Methods Western blot analysis, immunofluorescence staining and mass spectrometry in combination with laser capture microdissection to gain spatial resolution were used to characterise TG2 expression in the epithelial cell layer of healthy and coeliac disease affected duodenum. Findings TG2 is expressed in human duodenal epithelial cells, including cells in the apical region that are shed into the gut lumen. In untreated CeD the apical expression of TG2 is doubled. Enzymatically active TG2 is readily released from isolated human intestinal epithelial cells. Conclusion Shed epithelial cells are a plausible source of pathogenic TG2 enzyme in CeD. Increased epithelial TG2 expression and increased epithelial shedding in active CeD may reinforce action of luminal TG2 in this condition.

Se alle arbeider i NVA

• Sollid, Ludvig Magne (2026). Genetics of Celiac Disease: HLA and Beyond. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2026). T–Cell and B–Cell Crosstalk in the Development of Autoimmunity. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2026). What have we learned from trials in coeliac disease? Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2026). Triggering the Immune system: Transglutaminase in Celiac Disease and Inflammation. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2026). Autoimmunity seen through the lens of celiac disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2025). Impact of B cells as antigen presenting cells for the HLA association of celiac disease. Fulltekst i vitenarkiv
• Myklebust, June Helen; Sollid, Ludvig Magne & Tasken, Kjetil (2025). Oppdagelser om immunsystemet kan gi gjennombrudd i behandling av kreft og betennelsessykdommer. Aftenposten. Fulltekst i vitenarkiv
• Risnes, Louise Fremgaard; Dahal-Koirala, Shiva; Hjort, Rebecka; Bolstad, Nils; Lundin, Knut & Ness-Jensen, Eivind [Vis alle 7 forfattere av denne artikkelen] (2025). Detection of gluten-specific CD4+ T cells with tetramer test among anti-transglutaminase seropositive participants in the HUNT4 study. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2025). Involvement of gut luminal transglutaminase in the pathogenesis of celiac disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2025). Autoimmunity: Lessons to learn from celiac disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2025). B cell and T cell responses of the gut. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2025). From genetic risk to loss of immune tolerance: the pathophysiology of celiac disease . Fulltekst i vitenarkiv
• Hjort, Rebecka Louise; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). MAPPING OF HLA-DQ HAPLOTYPES IN ADULTS WITH COELIAC DISEASE IN A LARGE, SCREENED POPULATION – RESULTS FROM THE HUNT STUDY. Fulltekst i vitenarkiv
• Hjort, Rebecka Louise; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). MAPPING OF HLA-DQ HAPLOTYPES IN ADULTS WITH COELIAC DISEASE IN A LARGE, SCREENED POPULATION – RESULTS FROM THE HUNT STUDY. Gastroenterology. ISSN 0016-5085. 166(5), s. S-728–S-728. Fulltekst i vitenarkiv
• Hjort, Rebecka Louise; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). Mapping of HLA-DQ haplotypes in adults with coeliac disease in a large, screened population – results from the HUNT Study. Fulltekst i vitenarkiv
• Meling, Maureen Tania; Kleppa, Liv; Besser, Harrison; Khosla, Chaitan; Pré, Fleur du & Sollid, Ludvig Magne (2024). Enterocyte-Derived and Catalytically Active Transglutaminase 2 in the Gut Lumen of Mice: Implications for Celiac Disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). What have we learnt about coeliac disease and where should we go next? Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Pathogenic transglutaminases in gluten sensitive disorders. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Coeliac Disease: Gluten and transglutaminases. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). The maladapted immune response to gluten in celiac disease. Fulltekst i vitenarkiv
• Løberg, Runa Ingrunsdotter; Dewan, Alisa Elinsdatter; Kleppa, Liv; Pré, Fleur du & Sollid, Ludvig Magne (2024). Development of gluten-specific plasma cells in response to oral immunizations. Fulltekst i vitenarkiv
• Meling, Maureen Tania; Kleppa, Liv; Besser, Harrison; Khosla, Chaitan; Pré, Fleur du & Sollid, Ludvig Magne (2024). Enterocyte-Derived and Catalytically Active Transglutaminase 2 in the Gut Lumen of Mice: Implications for Celiac Disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Coeliac Disease. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Hjort, Rebecka Louise; Hveem, Kristian; Lundin, Knut; Jonkers, Iris H. & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). Assessing the susceptibility of celiac disease by polygenic risk scores: analysis of a population-based cohort, the HUNT study. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Hjort, Rebecka Louise; Thomas, Laurent Francois; Brumpton, Ben Michael; Hveem, Kristian & Lundin, Knut [Vis alle 9 forfattere av denne artikkelen] (2024). The IRX1 locus is associated with celiac disease: results from a screened population-based cohort, the HUNT study. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Hjort, Rebecka Louise; Hveem, Kristian; Lundin, Knut; Jonkers, Iris H. & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). Assessing the susceptibility of celiac disease by polygenic risk scores: analysis of a population-based cohort, the HUNT study. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Hjort, Rebecka Louise; Thomas, Laurent Francois; Brumpton, Ben Michael; Hveem, Kristian & Lundin, Knut [Vis alle 9 forfattere av denne artikkelen] (2024). The IRX1 locus is associated with celiac disease: results from a screened population-based cohort, the HUNT study. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Coeliac Disease: Gluten and transglutaminases. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). What have we learnt about coeliac disease and where should we go next? Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf; Warren, David John; Bolstad, Nils & Sollid, Ludvig Magne [Vis alle 8 forfattere av denne artikkelen] (2024). Serological signs of coeliac disease in pre-diagnostic samples from a population-based cohort of coeliacs, the Trøndelag Health Study (HUNT), Norway. Fulltekst i vitenarkiv
• Risnes, Louise Fremgaard; Dahal-Koirala, Shiva; Hjort, Rebecka Louise; Bolstad, Nils; Christophersen, Asbjørn Otto & Sarna, Vikas Kumar [Vis alle 9 forfattere av denne artikkelen] (2024). Påvisning av glutenspesifikke CD4+ T-celler med tetramertest blant anti-transglutaminase seropositive deltakere i HUNT4-studien. Fulltekst i vitenarkiv
• Hjort, Rebecka; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). MAPPING OF HLA-DQ HAPLOTYPES IN ADULTS WITH COELIAC DISEASE IN A LARGE, SCREENED POPULATION – RESULTS FROM THE NORWEGIAN HUNT STUDY. Fulltekst i vitenarkiv
• Hjort, Rebecka; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). Mapping of HLA-DQ haplotypes in adults with coeliac disease in a large, screened population – results from the Norwegian HUNT study. Fulltekst i vitenarkiv
• Hjort, Rebecka; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Sollid, Ludvig Magne & Ness-Jensen, Eivind [Vis alle 7 forfattere av denne artikkelen] (2024). MAPPING OF HLA-DQ HAPLOTYPES IN ADULTS WITH COELIAC DISEASE IN A LARGE, SCREENED POPULATION – RESULTS FROM THE NORWEGIAN HUNT STUDY. United European Gastroenterology Journal (UEG Journal). ISSN 2050-6406. 12(S8), s. 201–664. Fulltekst i vitenarkiv
• Hjort, Rebecka; Andersen, Ina Lervåg; Lukina, Polina; Hveem, Kristian; Lundin, Knut & Sollid, Ludvig Magne [Vis alle 7 forfattere av denne artikkelen] (2024). Mapping of HLA-DQ haplotypes in adults with coeliac disease in a large, screened population – results from the Norwegian HUNT study. Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf; Warren, David John; Bolstad, Nils & Iversen, Rasmus [Vis alle 9 forfattere av denne artikkelen] (2024). Serologiske tegn på cøliaki i pre-diagnostiske prøver fra en populasjonsbasert kohort av voksne cøliakere, Helseundersøkelsen i Trøndelag (HUNT). Fulltekst i vitenarkiv
• Dyrli, Ole Thomas; Andersen, Ina Lervåg; Lukina, Polina; Klaasen, Rolf; Bolstad, Nils & Warren, David John [Vis alle 9 forfattere av denne artikkelen] (2024). Anti-transglutaminase 2 immunoglobulin G in population-based screening for coeliac disease, the Trøndelag Health Study, Norway. United European Gastroenterology Journal (UEG Journal). ISSN 2050-6406. 12, s. 11–12. Fulltekst i vitenarkiv
• Dyrli, Ole Thomas; Andersen, Ina Lervåg; Lukina, Polina; Klaasen, Rolf; Bolstad, Nils & Warren, David John [Vis alle 9 forfattere av denne artikkelen] (2024). Anti-transglutaminase 2 immunoglobulin G in population-based screening for coeliac disease, the Trøndelag Health Study, Norway. Fulltekst i vitenarkiv
• Bostrøm, Stine; Uthaug, Lindis; Hjort, Rebecka Louise; Andersen, Ina Lervåg; Lukina, Polina & Sollid, Ludvig Magne [Vis alle 8 forfattere av denne artikkelen] (2024). Endoscopic findings in coeliac disease identified through population-based screening, the Trøndelag Health Study, Norway. United European Gastroenterology Journal (UEG Journal). ISSN 2050-6406. 12, s. 612–612. Fulltekst i vitenarkiv
• Bostrøm, Stine; Uthaug, Lindis; Hjort, Rebecka Louise; Andersen, Ina Lervåg; Lukina, Polina & Sollid, Ludvig Magne [Vis alle 8 forfattere av denne artikkelen] (2024). Endoscopic findings in coeliac disease identified through population-based screening, the Trøndelag Health Study, Norway. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Celiac disease -- a T-cell - B-cell driven immune disorder. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). On genes, environment and immune cells in autoimmune diseases. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2024). Celiac disease – a T-cell - B-cell driven immune disorder. Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf Anton; Warren, David; Bolstad, Nils & Sollid, Ludvig Magne [Vis alle 8 forfattere av denne artikkelen] (2023). SEROLOGICAL SIGNS OF COELIAC DISEASE IN PRE-DIAGNOSTIC SAMPLES FROM A POPULATION-BASED COHORT OF COELIACS, THE TRØNDELAG HEALTH STUDY (HUNT), NORWAY. United European Gastroenterology Journal (UEG Journal). ISSN 2050-6406. 11. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Recent developments and future paths in celiac immunology. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Immunologic and genetic responses in celiac disease . Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Mucosal immune responses in Celiac Disease. Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf Anton; Warren, David; Iversen, Rasmus & Mjønes, Patricia Gjertrud [Vis alle 11 forfattere av denne artikkelen] (2023). THE TOTAL PREVALENCE AND RATE OF UNDIAGNOSED CELIAC DISEASE IN AN ADULT GENERAL POPULATION – THE HUNT STUDY, NORWAY. Gastroenterology. ISSN 0016-5085. 164(6), s. S-218–S-218. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Gut Plasma Cells and Their Role in Celiac Disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). On the HLA association of celiac disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Celiac disease as a model for autoimmunity . Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Role of T Cell and B Cell Interactions in Autoimmunity: Lessons from Celiac Disease. Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Everything You Always Wanted to Know About Celiac Disease (But Were Afraid to Ask). Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Cøliaki som modell for autoimmune sykdommer . Fulltekst i vitenarkiv
• Sollid, Ludvig Magne (2023). Immunopathogenesis of celiac disease: Current wisdom and therapeutic exploitation. Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf Anton; Warren, David J; Bolstad, Nils & Mjønes, Patricia Gjertrud [Vis alle 11 forfattere av denne artikkelen] (2023). Prevalensen av cøliaki i den generelle befolkningen (HUNT4). Fulltekst i vitenarkiv
• Lukina, Polina; Andersen, Ina Lervåg; Klaasen, Rolf Anton; Warren, David; Iversen, Rasmus & Mjønes, Patricia Gjertrud [Vis alle 11 forfattere av denne artikkelen] (2023). THE TOTAL PREVALENCE AND RATE OF UNDIAGNOSED CELIAC DISEASE IN AN ADULT GENERAL POPULATION – THE HUNT STUDY, NORWAY. Fulltekst i vitenarkiv
• Alam, Mohammad Sayeef; Ness-Jensen, Eivind; Hjort, Rebecka; Sollid, Ludvig Magne & Lundin, Knut (2026). The genetic and environmental susceptibility for celiac disease. Norges teknisk-naturvitenskapelige universitet. ISSN 9788232698332. Fulltekst i vitenarkiv Vis sammendrag

  Celiac disease (CeD) is a lifelong immune-mediated condition that affects genetically susceptible individuals worldwide and is triggered by consuming gluten, a protein found in wheat, rye, and barley. It presents with a wide range of symptoms, from mild gastrointestinal complaints like bloating, constipation and stomach pain to severe complications such as anemia, osteoporosis, and infertility. Among adults, atypical symptoms like fatigue, brain fog, and mental distress are more common, leading to misdiagnosis or remaining undiagnosed, contributing to the iceberg like nature of CeD. In Norway, biopsy-confirmed diagnosis is double the global average, with 55% of these being previously undiagnosed. Fortunately, awareness of the disease and advancements in diagnostic technologies have led to increasing detection rates in recent studies. Currently, the only treatment is strict adherence to a gluten-free diet. The Trøndelag Health Study (HUNT4), conducted between 2017 and 2019 in Nord-Trøndelag County, Norway, invited 103,000 adults (aged ≥20 years) to participate. A total of 56,042 individuals participated, 54.6% of whom were women. HUNT is a unique longitudinal database of questionnaire data, clinical measurements and samples from the county’s inhabitants from 1984. From HUNT2 onwards, all biological samples were genotyped, providing a rich resource of genetic data. From HUNT4, 826 individuals were identified as biopsy-confirmed eD, of these 361 were identified through hospital-based medical journal searches, and 465 individuals were newly diagnosed. With genetic information, also available for all individuals from HUNT4, we performed genome-wide association analysis, polygenic risk scoring for comparison between the two groups, and finally tested a clinical prediction model corporating genetics, lifestyle, symptoms, comorbidities, and biomarkers to aid clinicians. A novel locus in a non-protein-coding region (5p15.33) was identified, adding to the 42 previously known loci. On average, individuals with CeD had a PRS of 1.7 units, placing them at 3.5 times higher risk compared to the general population. The previously known cases and newly diagnosed cases were comparable based on the genetic risk load that carry both at an aggregated PRS level as well as at variant level. PRS had a slightly higher (comparable) discriminatory power compared to the HLA haplotypes. Finally, clinical aid achieved high discrimination between cases and healthy individuals. The model at low predicted risk probability was able to capture more actual cases compared to general population screening. In conclusion, this thesis sets out to explore the genetic and environmental underpinnings of celiac disease in a large, population-based cohort, and it has yielded several important findings. The study confirmed that genetic variants associated with CeD are not limited to protein-coding or immune-specific regions, highlighting the relevance of non-coding loci such as 5p15.33. It also demonstrated that both newly detected and previously undiagnosed individuals carry similar genetic risk, distinguishing them from non-cases. By leveraging polygenic risk scores, the study established a strong association between genetic predisposition and CeD. The combination of genetic and non-genetic factors further enhances case detection at true population prevalence settings. The study is limited with lack of external validation for the genetic findings as well as for the clinical prediction model. Future studies require more ethnically diverse population, with longitudinal information on environmental factors to determine causal pathways outside genetics. This would enhance the understanding the disease and prevent and manage the disease better.

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