Premium
Interleukin‐17‐producing γδ + T cells protect NOD mice from type 1 diabetes through a mechanism involving transforming growth factor‐β
Author(s) -
Han Gencheng,
Wang Renxi,
Chen Guojiang,
Wang Jianan,
Xu Ruonan,
Wang Liyan,
Feng Jiannan,
Li Xia,
Guo Renfeng,
Fu Li,
Shen Beifen,
Li Yan
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03166.x
Subject(s) - nod , adoptive cell transfer , nod mice , immunology , diabetes mellitus , pathogenesis , splenocyte , biology , immune system , t cell , endocrinology
Summary Whether interleukin (IL)‐17 promotes a diabetogenic response remains unclear. Here we examined the effects of neutralization of IL‐17 on the progress of adoptively transferred diabetes. IL‐17‐producing cells in non‐obese diabetic (NOD) mice were identified and their role in the pathogenesis of diabetes examined using transfer and co‐transfer assays. Unexpectedly, we found that in vivo neutralization of IL‐17 did not protect NOD–severe combined immunodeficiency (SCID) mice against diabetes transferred by diabetic splenocytes. In NOD mice, γδ + T cells were dominated by IL‐17‐producing cells and were found to be the major source of IL‐17. Interestingly, these IL‐17‐producing γδ T cells did not exacerbate diabetes in an adoptive transfer model, but had a regulatory effect, protecting NOD mice from diabetes by up‐regulating transforming growth factor (TGF)‐β production. Our data suggest that the presence of IL‐17 did not increase the chance of the development of diabetes; γδ T cells protected NOD mice from diabetes in a TGF‐β‐dependent manner, irrespective of their role as major IL‐17 producers.