Abstract
The involvement of natural killer (NK) cells in the development of diabetes in the normally resistant 9-10 week old C57BL/6J male mice by the D variant of encephalomyocarditis virus (EMCV-D) was examined. Inoculation of purified EMCV-D induced maximum NK cell activity in splenic cell populations on day 4 post-inoculation as determined by lysis of YAC-1 target cells in a standard 51chromium release microcytotoxicity assay. Selective depletion of NK cells by the administration of rabbit anti-asialo GM1 sera prior to challenging the C57BL/6J mice with EMCV-D, resulted in diminished splenic NK cell activity, increased EMCV-D viral titers in the pancreas, spleen, heart and brain, and the induction of diabetes in 60-80% of the mice. The data suggest that NK cells play a role in host protection against the diabetogenic EMCV-D.
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