title: Polymorphonuclear neutrophils enhance suppressive activities of anti-CD3-induced CD4+ suppressor T cells.
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.
authors.affiliation: Second Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hirohata
authors.forename: T
authors.initials: T
authors.lastname: Yanagida
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshino
authors.forename: H
authors.initials: H
authors.lastname: Miyashita
mesh_terms: D000328:Adult; D000917:Antibody Formation; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D002450:Cell Communication; D002478:Cells, Cultured; D005404:Fixatives / Q000494:pharmacology; D005557:Formaldehyde / Q000494:pharmacology; D006801:Humans; D007075:Immunoglobulin M / Q000096:biosynthesis / Q000235:genetics; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics / Q000494:pharmacology; D016685:Mitomycin / Q000494:pharmacology; D016853:Muromonab-CD3 / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology*; D011108:Polymers / Q000494:pharmacology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism
chemical_list: D005404:Fixatives; D007075:Immunoglobulin M; D007376:Interleukin-2; D016853:Muromonab-CD3; D011108:Polymers; D005557:Formaldehyde; D016685:Mitomycin; C003043:paraform