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    Jefferson Adams
    Jefferson Adams

    Gluten May Play Role in Triggering Type 1 Diabetes

    Reviewed and edited by a celiac disease expert.
    Gluten May Play Role in Triggering Type 1 Diabetes - Photo: CC - woodleywonderworks
    Caption: Photo: CC - woodleywonderworks

    Celiac.com 11/21/2011 - Celiac disease is common in people with type 1 diabetes (T1D). These people can show Abs reactions against tissue transglutaminase, the prime trigger in celiac disease. In short, gliadin seems to play a role in type 1 diabetes pathogenesis.

    An international research team set out to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D.

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    Photo: CC - woodleywonderworksThe researchers included Heather J. Galipeau, Nestor E. Rulli, Jennifer Jury, Xianxi Huang, Romina Araya, Joseph A. Murray, Chella S. David, Fernando G. Chirdo, Kathy D. McCoy, and Elena F. Verdu, and are variously affiliated with the Farncombe Family Digestive Health Research Institute at McMaster University Medical Centre in Canada, Laboratorio de Investigación en el Sistema Inmune, Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Argentina, the Department of Internal Medicine, and the Department of Immunology at the Mayo Clinic College of Medicine in Rochester, MN, and with the Department of Clinical Research, University of Bern, Bern, Switzerland.

    Researchers know that gliadin-sensitized NOD-DQ8 mice develop moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but do not develop insulitis. The team administered anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25+Foxp3+ T cells, which triggered severe insulitis, but did not worsen mucosal dysfunction.

    The team isolated CD4+ T cells isolated from pancreatic lymph nodes. Those from mice that developed insulitis showed higher proliferation and pro-inflammatory cytokines after incubation with gliadin, but not with BSA. CD4+ T cells isolated from non-sensitized control mice showed no response to gliadin or BSA.

    From these observations, the team concluded that gliadin sensitization triggered moderate enteropathy in NOD-DQ8 mice. However, triggering insulitis required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T cells.

    This study offers a model for explaining how mucosal intolerance to a dietary protein can trigger insulitis as a result of partial regulatory T cell deficiency.

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  • About Me

    Jefferson Adams

    Jefferson Adams is Celiac.com's senior writer and Digital Content Director. He earned his B.A. and M.F.A. at Arizona State University. His articles, essays, poems, stories and book reviews have appeared in numerous magazines, journals, and websites, including North American Project, Antioch Review, Caliban, Mississippi Review, Slate, and more. He is the author of more than 2,500 articles on celiac disease. His university coursework includes studies in science, scientific methodology, biology, anatomy, physiology, medicine, logic, and advanced research. He previously devised health and medical content for Colgate, Dove, Pfizer, Sharecare, Walgreens, and more. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of numerous books, including "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

    >VIEW ALL ARTICLES BY JEFFERSON ADAMS

     


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