The suppressive effect of anti-asialo GM1 antibody on low-dose streptozotocin-induced diabetes in CD-1 mice.

To elucidate the role of natural killer (NK) cells in the pathogenesis of diabetes in streptozotocin-induced diabetes, we examined whether treatment with anti-asialo GM1 antibody prevents the occurrence of diabetes in CD-1 mouse model. Anti-asialo GM1 antibody was injected intraperitoneally 2-3 times a week starting three days before the first streptozotocin injection. In controls, rabbit immunoglobulin or saline was injected instead of anti-asialo GM1 antibody. Three of twelve anti-asialo GM1 antibody-treated mice developed diabetes, however eight of eight (100%) rabbit immunoglobulin injected mice and 20 of 23 saline-injected mice developed diabetes. The incidence of diabetes in the anti-asialo GM1 antibody-injected group was significantly higher than in the two control groups (p less than 0.01, p less than 0.01, respectively). The NK-cell activities of spleen cells from anti-asialo GM1 antibody-treated mice were significantly lower than in control mice. Flow-cytometry analysis demonstrated that anti-asialo GM1 antibody-positive cells had disappeared from spleens of anti-asialo GM1 antibody-injected mice but no suppression of T-lymphocytes could be demonstrated. These results suggest that NK cells play a role in the pathogenesis of streptozotocin-induced diabetes in CD-1 mice.