Cell-mediated cytotoxicity against ectromelia virus-infected target cells. I. Specificity and kinetics

Spleen cells from mice immunized intravenously with attenuated ectromelia virus were cytotoxic for target cells infected with virulent ectromelia virus in the absence of exogenous complement; cytotoxicity was measured by ⁵¹Cr release from target cells. L929 cells were the most sensitive target cells, but the effect could also be demonstrated with P-815 mastocytoma cells and chick embryo cells; mouse embryo cells were unsatisfactory. Hyperimmune anti-ectromelia serum and complement was not significantly cytotoxic although fluorescein-conjugated antiserum stained virus-infected L929 cells. Release of ⁵¹Cr label from ectromelia-immune spleen cells (at a spleen cell: target cell ratio of 100: 1) increased in a linear manner with time, until a plateau was reached at 20–24 hours. Cytotoxicity appeared to be specific in that ectromelia-immune spleen cells killed ectromelia-infected L929 cells, but not uninfected L929 cells, whereas spleen cells from mice immunized with Listeria monocytogenes (a potent stimulus for cell-mediated immunity) or from normal mice, did not kill ectromelia-infected L929 cells. Spleen cells from mice immunized with vaccinia virus (a poxvirus closely related to ectromelia) were cytotoxic for ectromelia-infected L929 cells. Spleen cells from mice immunized with ectromelia virus had acquired cytotoxic activity by 2 days after immunization. Cytotoxic potency reached a peak at 6 days and had declined to a low level by day 10. The potential significance of the phenomenon in relation to control of viral infection is discussed.