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SOCS-1 protects from virally-induced CD8 T cell mediated type 1 diabetes.

Abstract：

:CD8(+) cytotoxic T lymphocytes (CTL) can rapidly kill beta-cells and therefore contribute to the development of type 1 diabetes (T1D). CTL-mediated beta-cell killing can occur via perforin-mediated lysis, Fas-Fas-L interaction, and the secretion of TNF-alpha or IFN-gamma. The secretion of IFN-gamma can contribute to beta-cell death directly by eliciting nitric oxide production, and indirectly by upregulating MHC class I and 'unmasking' beta-cells for recognition by CTL. Earlier studies in the RIP-LCMV mouse model of diabetes showed that disruption of beta-cell IFN-gamma signaling alone abolished the direct detrimental effects of IFN-gamma, but not MHC class I upregulation. Suppressor of cytokine signaling-1 (SOCS-1) represses several crucial cytokine signaling pathways simultaneously, among them IFN-gamma and IL-1-beta. We therefore evaluated the protective capacity of islet cell SOCS-1 expression in the CD8(+) mediated RIP-LCMV diabetes model. Clinical disease was prevented in over 90% of the mice. Not only absence of MHC-I and Fas upregulation, but also resistance to cytokine-induced killing of beta-cells and a complete lack of CXCL-10 (IP10) production in islets led to a lack of islet infiltration and impaired activation of autoaggressive CD4(+) and CD8(+) T-cells in these mice. Thus, SOCS expression renders beta-cells resistant to CTL attack in a mouse model of T1D.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

Barral AM,Thomas HE,Ling EM,Darwiche R,Rodrigo E,Christen U,Ejrnaes M,Wolfe T,Kay TW,von Herrath MG

doi

10.1016/j.jaut.2006.08.002

subject

Has Abstract

pub_date

2006-11-01 00:00:00

pages

166-73

issue

3

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(06)00073-4

journal_volume

27

pub_type

杂志文章

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