Inflammatory process in murine lymphocytic choriomeningitis is maximal in H-2K or H-2D compatible interactions.

Capacity to transfer adoptively fatal lymphocytic choriomeningitis (LCM) to immunosuppressed, virus-infected recipients is a property of H-2 compatible, non-Ig-bearing virus-immune lymphocytes. Severe meningitis is recognized when donor and recipient share at least one allele at either H-2K or H-2D. Presence of unshared H-2 genes is not obviously inhibitory, and identity at the immune response (Ir) region of the H-2 gene complex is neither sufficient nor necessary. The same constraint applies to cytotoxic T cell activity in vitro; lymphocytes and virus-infected targets must be compatible for a minimum of one allele mapping at H-2K or H-2D. The present findings thus support the concept that populations of T cells, which are cytotoxic in vitro, also mediate inflammatory process in vivo and are a major, if not the only, effector population in murine LCM.