Abstract
Adoptive transfer of anti-Listeria resistance by Listeria-immune spleen T cells was markedly reduced by pretreatment of the cells with monoclonal anti-Lyt 2.2 and complement (Lyt 2+C); pretreatment of cells with monoclonal anti-L3T4 and complement (L3T4+C) had a lesser effect on their ability to transfer resistance. Lyt 2+C-treated and L3T4+C-treated Listeria-immune T cells were undiminished in their immediate ability to transfer enhanced accumulation of inflammatory peritoneal neutrophils and macrophages in response to Listeria antigens. When L3T4+C- and Lyt 2+C-treated Listeria-immune spleen cells were cultured in vitro before transfer, however, it became apparent that the L3T4+ subset was particularly important for mediating in vivo accumulation of inflammatory phagocytes. Listeria-immune spleen T cells produced soluble factors during in vitro culture that, when injected i.p., were able to recruit inflammatory neutrophils and macrophages to the peritoneal cavities of recipient mice. Pretreatment of Listeria -immune spleen cells with L3T4+C before culture markedly diminished their ability to produce soluble factors that were capable of attracting neutrophils and macrophages in vivo. The results of this study indicate substantial roles for both Lyt 2+ and L3T4+ T-cell subsets in the dual regulation of inflammation and anti-bacterial resistance; Lyt 2+ T cells appear to be the principal mediator of anti-bacterial resistance, whereas L3T4+ T cells augment the recruitment of inflammatory phagocytes in vivo.
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