Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetes–prone mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-12

AUTHORS

J Tian, M Clare-Salzler, A Herschenfeld, B Middleton, D Newman, R Mueller, S Arita, C Evans, M A Atkinson, Y Mullen, N Sarvetnick, A J Tobin, P V Lehmann, D L Kaufman

ABSTRACT

In nonobese diabetic (NOD) mice, beta-cell reactive T-helper type 1 (Th1) responses develop spontaneously and gradually spread, creating a cascade of responses that ultimately destroys the beta-cells. The diversity of the autoreactive T-cell repertoire creates a major obstacle to the development of therapeutics. We show that even in the presence of established Th1 responses, it is possible to induce autoantigen-specific anti-inflammatory Th2 responses. Immune deviation of T-cell responses to the beta-cell autoantigen glutamate decarboxylase (GAD65), induced an active form of self-tolerance that was associated with an inhibition of disease progression in prediabetic mice and prolonged survival of syngeneic islet grafts in diabetic NOD mice. Thus, modulation of autoantigen-specific Th1/Th2 balances may provide a minimally invasive means of downregulating established pathogenic autoimmune responses. More... »

PAGES

1348

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm1296-1348

DOI

http://dx.doi.org/10.1038/nm1296-1348

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1015991784

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8946834


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