β2-microglobulin–deficient NOD mice do not develop insulitis or diabetes

LS Wicker, EH Leiter, JA Todd, RJ Renjilian… - Diabetes, 1994 - Am Diabetes Assoc
LS Wicker, EH Leiter, JA Todd, RJ Renjilian, E Peterson, PA Fischer, PL Podolin, M Zijlstra…
Diabetes, 1994Am Diabetes Assoc
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 β-cell destruction. To assess the
contribution of CD8+ T-cells to diabetes, we have developed a class of NOD mouse that
lacks expression of βxs2-microglobulin (NOD-B2m null). NOD-B2m null mice, which lack …
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 β-cell destruction. To assess the contribution of CD8+ T-cells to diabetes, we have developed a class of NOD mouse that lacks expression of βxs2-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 β-cells in the NOD mouse.
Am Diabetes Assoc