Natural killer cells contribute to inflammation but do not appear to be essential for the induction of clinical lymphocytic choriomeningitis.

The inflammatory exudate found in cerebrospinal fluid (CSF) of mice 6 days after intracerebral infection with lymphocytic choriomeningitis virus (LCMV) contains substantial populations of both cytotoxic T lymphocytes (CTL) and natural killer (NK) cells. Removal of NK cell activity by in vivo treatment with antibody to the asialo GM1 ganglioside and studies with NK-deficient bg/bg mice did not clearly determine whether NK cells contribute in any way to the development of clinical LCM. However, the LCM disease process induced in cyclophosphamide-suppressed, LCMV-infected recipients by the adoptive transfer of LCMV-immune spleen cells occurs in the absence of NK cell effector function in spleen, lymph nodes, or CSF of the recipients, though potent CTL populations are present in all of these sites. In this situation, NK cells are apparently not required for the induction of neurological symptoms that are indistinguishable from those of classical LCM.