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Peritoneal exudate T lymphocytes fromListeria monocytogenes -immune mice in the presence of the homologous antigen (heat-killedL. monocytogenes ) and normal macrophages showedL. monocytogenes -specific proliferative responses. Proliferation was inhibited by macrophages fromL. monocytogenes - orCorynebacterium parvum -pretreated mice as well as by exogenous prostaglandin E2 . Macrophage-dependent inhibition of T-cell proliferation—at least in part—could be reversed by addition of indomethacin. When selectedL. monocytogenes -immune Lyt T-cell subsets were cultured in the presence of inhibitory macrophages, pretreatment with anti-Lyt 1 antiserum plus complement completely abrogated proliferation and pretreatment with anti-Lyt 2 and anti-Lyt 3 antisera plus complement markedly reduced proliferation. However, a mixture (1:1) of the two preselected Lyt T-cell subsets resulted in complete reconstitution of proliferative responses. In contrast, whenL. monocytogenes -immune peritoneal exudate T lymphocytes were treated with anti-Lyt antisera plus complement after culture, only treatment with anti-Lyt 1 antiserum plus complement affected proliferation, suggesting regulatory interactions between Lyt 1+ 23− and Lyt 1− 23+ T cells during in vitro culture which result in proliferation within the Lyt 1+ 23− T-cell subset. After rigorous depletion of residual macrophages and in the presence of indomethacin, pretreatment with anti-Lyt 1 antiserum plus complement, but not with anti-Lyt 2 and 3 antisera plus complement, eliminated proliferation. The data presented indicate that interactions between macrophages and Lyt T-cell subsets regulateL. monocytogenes -specific T-cell activation.

Regulatory Interactions Between Macrophages and T-Cell Subsets in Listeria monocytogenes -Specific T-Cell Activation