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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetes-prone mice.

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.[1]

References

  1. Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetes-prone mice. Tian, J., Clare-Salzler, M., Herschenfeld, A., Middleton, B., Newman, D., Mueller, R., Arita, S., Evans, C., Atkinson, M.A., Mullen, Y., Sarvetnick, N., Tobin, A.J., Lehmann, P.V., Kaufman, D.L. Nat. Med. (1996) [Pubmed]
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