Intracranial infection of normal mice with lymphocytic choriomeningitis virus (LCMV) causes meningitis and death mediated by CD8+ major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes (CTLs). β2-Microglobulin-deficient mice (ß 2M-/-) do not express functional MHC class I proteins and do not produce significant numbers of CD8+ T cells. When β2M-/- mice were infected with LCMV, many died from LCMV disease and produced a specific response to LCMV mediated by CD4 + CTLs that were class II-restricted. In these mice, CD4+ CTLs may compensate for the lack of CD8+ CTLs.
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