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题目:: Mouse pancreatic beta cells express MHC class II and stimulate CD4(+) T cells to proliferate.
作者:: Zhao(Yuxing),Scott(Nicholas A),Quah(Hong Sheng),Krishnamurthy(Balasubramanian),Bond(Francene),Loudovaris(Thomas),Mannering(Stuart I),Kay(Thomas W H),Thomas(Helen E)
状态:: 发布时间2015-09-08 , 更新时间 2015-09-08
期刊:: Eur J Immunol
摘要:: Type 1 diabetes results from destruction of pancreatic beta cells by autoreactive T cells. Both CD4(+) and CD8(+) T cells have been shown to mediate beta-cell killing. While CD8(+) T cells can directly recognize MHC class I on beta cells, the interaction between CD4(+) T cells and beta cells remains unclear. Genetic association studies have strongly implicated HLA-DQ alleles in human type 1 diabetes. Here we studied MHC class II expression on beta cells in nonobese diabetic mice that were induced to develop diabetes by diabetogenic CD4(+) T cells with T-cell receptors that recognize beta-cell antigens. Acute infiltration of CD4(+) T cells in islets occurred with rapid onset of diabetes. Beta cells from islets with immune infiltration expressed MHC class II mRNA and protein. Exposure of beta cells to IFN-γ increased MHC class II gene expression, and blocking IFN-γ signaling in beta cells inhibited MHC class II upregulation. IFN-γ also increased HLA-DR expression in human islets. MHC class II(+) beta cells stimulated the proliferation of beta-cell-specific CD4(+) T cells. Our study indicates that MHC class II molecules may play an important role in beta-cell interaction with CD4(+) T cells in the development of type 1 diabetes.
语言:: eng
DOI:: 10.1002/eji.201445378

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