Figure 1. Immunopathogenesis of celiac disease. Following gluten consumption, gluten proteins are partially digested into immunogenic peptides that resist complete proteolysis in the lumen of the small intestine. These peptides cross the intestinal epithelium and are deamidated by tissue transglutaminase (TG2), increasing their affinity for HLA-DQ2/8 molecules on antigen-presenting cells. Deamidated gluten peptides are presented to CD4⁺ T cells, leading to their activation and the release of pro-inflammatory cytokines (e.g., IFN-γ, IL-21). Activated T cells provide help to B cells, promoting differentiation into plasma cells that produce anti-gluten and anti-TG2 antibodies.

References

1. Lindfors, K., Ciacci, C., Kurppa, K., Lundin, K. E. A., Makharia, G. K., Mearin, M. L., Murray, J. A., Verdu, E. F., & Kaukinen, K. (2019). Coeliac disease. Nature Reviews Disease Primers, 5(1), 3. https://doi.org/10.1038/s41572-018-0054-z