Faculty Research 1990 - 1999

Beta 2-microglobulin-deficient NOD mice do not develop insulitis or diabetes.

Document Type

Article

Publication Date

1994

Keywords

Animal, Antigens-CD8: an, Autoimmune-Diseases: im, Base-Sequence, Diabetes-Mellitus-Experimental: im, Female, Islets-of-Langerhans: im, Mice, Mice-Inbred-NOD, Molecular-Sequence-Data, Spleen: cy, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes: im, tr

First Page

500

Last Page

504

JAX Source

Diabetes 1994 Mar;43(3):500-4

Grant

DK27722/DK/NIDDK, DK36175/DK/NIDDK

Abstract

The role of CD8+ T-cells in the development of diabetes in the nonobese diabetic (NOD) mouse remains controversial. Although it is widely agreed that class II-restricted CD4+ T-cells are essential for the development of diabetes in the NOD model, some studies have suggested that CD8+ T-cells are not required for beta-cell destruction. To assess the contribution of CD8+ T-cells to diabetes, we have developed a class of NOD mouse that lacks expression of beta 2-microglobulin (NOD-B2mnull). NOD-B2mnull mice, which lack both class I expression and CD8+ T-cells in the periphery, not only failed to develop diabetes but were completely devoid of insulitis. These results demonstrate an essential role for CD8+ T-cells in the initiation of the autoimmune response to beta-cells in the NOD mouse.

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