ArticleMucosal immunology2011
Single-chain recombinant HLA-DQ2.5/peptide molecules block α2-gliadin-specific pathogenic CD4+ T-cell proliferation and attenuate production of inflammatory cytokines: a potential therapy for celiac disease.
Article in Mucosal immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Celiac Disease: A Review from Genetic to Treatment.Iranian biomedical journal · 2024Review
- Celiac disease: mechanisms and emerging therapeutics.Trends in pharmacological sciences · 2023Review
- Unraveling the Immunopathological Landscape of Celiac Disease: A Comprehensive Review.International journal of molecular sciences · 2023Review
- New Developments in Celiac Disease Treatment.International journal of molecular sciences · 2023Review
- Therapeutic approaches for celiac disease.Best practice & research. Clinical gastroenterology · 2015Review
- Dissection of the human multipotent adult progenitor cell secretome by proteomic analysis.Stem cells translational medicine · 2013Article
- Effective Arrestin-Specific Immunotherapy of Experimental Autoimmune Uveitis with RTL: A Prospect for Treatment of Human Uveitis.Translational vision science & technology · 2013Article
- Pulse-chase analysis for studies of MHC class II biosynthesis, maturation, and peptide loading.Methods in molecular biology (Clifton, N.J.) · 2013Article
- The immunopathogenesis of celiac disease reveals possible therapies beyond the gluten-free diet.Seminars in immunopathology · 2012Review
- Peptide-MHC-based nanovaccines for the treatment of autoimmunity: a "one size fits all" approach?Journal of molecular medicine (Berlin, Germany) · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Celiac disease (CD) is a disorder of the small intestine caused by intolerance to wheat gluten and related proteins in barley and rye. CD4(+) T cells have a central role in CD, recognizing and binding complexes of HLA-DQ2.5 bearing gluten peptides that have survived digestion and that are deamidated by tissue transglutaminase (TG2), propagating a cascade of inflammatory processes that damage and eventually destroy the villous tissue structures of the small intestine. In this study, we present data showing that recombinant DQ2.5-derived molecules bearing covalently tethered α2-gliadin-61-71 peptide have a remarkable ability to block antigen-specific T-cell proliferation and inhibited proinflammatory cytokine secretion in human DQ2.5-restricted α2-gliadin-specific T-cell clones obtained from patients with CD. The results from our in vitro studies suggest that HLA-DQ2.5-derived molecules could significantly inhibit and perhaps reverse the intestinal pathology caused by T-cell-mediated inflammation and the associated production of proinflammatory cytokines.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.