Abstract:
:Non-obese diabetic (NOD) mice develop spontaneous T-cell responses against pancreatic beta-cells, leading to islet cell destruction and diabetes. Despite high genetic similarity, non-obese resistant (NOR) mice do not develop diabetes. We show here that spleen cells of both NOD and NOR mice respond to the islet cell antigen glutamic acid decarboxylase-65 in IFN-gamma-ELISPOT assays. Moreover, NOR-T cells induce periinsulitis in NOD SCID recipient mice. Thus, a potentially pathogenic islet cell-specific T-cell response arises in NOR and NOD mice alike; the mechanism that prevents the autoimmune progression of self-reactive T cells in NOR mice presumably acts at the level of effector function. Consistent with this hypothesis, CD4+CD25+ cell-depleted spleen cells from NOR mice mediated islet cell destruction and overt diabetes in NOD SCID mice. Therefore, islet cell-specific effector cells in NOR mice appear to be under the control of CD4+CD25+ regulatory T cells, confirming the importance of regulatory cells in the control of autoimmune diabetes.
journal_name
Cell Immunoljournal_title
Cellular immunologyauthors
Ott PA,Anderson MR,Tary-Lehmann M,Lehmann PVdoi
10.1016/j.cellimm.2005.05.003subject
Has Abstractpub_date
2005-05-01 00:00:00pages
1-11issue
1eissn
0008-8749issn
1090-2163pii
S0008-8749(05)00088-2journal_volume
235pub_type
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更新日期:2011-01-01 00:00:00
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