Abstract
Abstract Cytotoxic capacity of immune CBA/H spleen cells for monolayers of L cells infected with lymphocytic choriomeningitis (LCM) virus is abrogated by prior incubation with AKR anti-ϑ ascitic fluid and complement, but is unaffected by treatment with anti-mouse-Ig serum and complement. Depletion of splenic macrophages, or addition of normal or activated (from listeria-immune mice) peritoneal macrophages, does not significantly modify the activity of immune spleen cells. Cell-mediated release of 51Cr from LCM-infected targets may thus be attributed to thymus-derived effector lymphocytes (T cells). Such T cells are specific insofar as they do not exhibit cytotoxic activity for monolayers infected with ectromelia virus, which are readily lysed by homologous immune cells. Development of cytotoxic lymphocytes is related to the dose of virus given: injection of high concentrations leads to peak activity on day 5. Maximal cytotoxicity is, however, mediated by spleen cells taken on day 7 from mice immunized with a relatively small dose of virus.
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