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Inflammatory Process in Murine Lymphocytic Choriomeningitis Is Maximal in H-2K or H-2D Compatible Interactions

From the Department of Microbiology, The John Curtin School of Medical Research, Canberra A.C.T., Australia

Abstract

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.

Footnotes

¹ Present address: The Wistar Institute, 36th Street at Spruce, Philadelphia, Pennsylvania 19104.

² Present address: Scripps Clinic and Research Foundation, La Jolla, California 92037.

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