Lyt-2+ T cell-mediated protection against listeriosis. Protection correlates with phagocyte depletion but not with IFN-gamma production.

The transfer of listeria-immune splenocytes into non-immune mice markedly increases host resistance to listeriosis. To study the mechanism for this enhancement, we compared the inflammatory response to infection in nonimmune and adoptively immunized mice. Despite much better containment of bacterial growth, adoptively immunized animals accumulated significantly fewer phagocytes (neutrophils and macrophages) in the spleen and liver than controls. Immune T cells not only inhibited phagocyte accumulation but also reduced the in vitro anti-listerial activity of splenocytes. Significant differences in phagocyte accumulation were observed even when the initial listeria dose was adjusted to produce comparable spleen listeria loads in immune and non-immune animals. However, bone marrow and peripheral blood phagocyte counts were similar in both groups. Depletion of Lyt-2+ cells (using mAb and C) from donor splenocytes prevented the transfer of protection and increased phagocyte accumulation without altering listeria-dependent IFN-gamma production by donor or recipient splenocytes in vitro. L3T4 depletion did not affect host resistance or phagocyte accumulation even though it reduced in vitro interferon production by donor cells. Hence the different effects of L3T4+ and Lyt-2+ cells in vivo cannot be explained simply by variations in IFN production. We suggest this paradoxical suppression of phagocyte accumulation during adoptive transfer may reflect lysis of bacteria-laden phagocytes by listeria-specific Lyt-2+ cells in vivo. Selective destruction of older, heavily infected cells might contribute to host resistance by eliminating a potential site for intracellular proliferation of bacteria.