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. 1995 Feb;160(2):270-7.
doi: 10.1016/0008-8749(95)80038-k.

Polymorphonuclear neutrophils enhance suppressive activities of anti-CD3-induced CD4+ suppressor T cells

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Polymorphonuclear neutrophils enhance suppressive activities of anti-CD3-induced CD4+ suppressor T cells

S Hirohata et al. Cell Immunol. 1995 Feb.

Abstract

We investigated the effects of polymorphonuclear neutrophils (PMN) on the suppressive activities of CD4+ suppressor T cells induced by immobilized mAb to the CD3 molecular complex in order to explore the role of PMN in the regulation of humoral immune responses. CD4+ T cells that had been treated with mitomycin C induced the IgM production from highly purified B cells in cultures stimulated with immobilized anti-CD3. Addition of CD4+ T cells that had not been treated with mitomycin C (control T4 cells) suppressed the IgM production induced by immobilized anti-CD3-stimulated T4 mito. PMN enhanced the degree of suppression of the IgM production by anti-CD3-stimulated control T4 cells. The capacity of PMN to enhance the suppressive activity of anti-CD3-stimulated control T4 cells was restored when PMN were fixed with paraformaldehyde (PFA), suggesting that direct interactions between PMN and CD4+ T cells, but not soluble factors secreted by PMN, were involved in the enhancement of suppression. Fresh PMN as well as PFA-fixed PMN enhanced the endogenous IL-2 production by immobilized anti-CD3-stimulated CD4+ T cells. Moreover, neither fresh PMN nor PFA-fixed PMN significantly augmented the suppressive activity of anti-CD3-stimulated control T4 cells in the presence of exogenous IL-2. These results indicate that PMN enhance the suppressive activity of anti-CD3-stimulated control T4 cells through direct interactions between PMN and CD4+ T cells. The enhancement of the suppressive activity of CD4+ suppressor T cells by PMN is accounted for by the enhancement of the endogenous IL-2 production by anti-CD3-stimulated CD4+ T cells. Thus, the data demonstrate that PMN influence the magnitude of humoral immune responses by regulating the production of IL-2 through direct interactions with T cells.

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