Divergent T gamma cell functions in antigen-induced blastogenesis: facilitory interactions with Tnon gamma cells and participation in monocyte- and prostaglandin-mediated suppression.
The contribution of T gamma cells, i.e., T cells bearing surface receptors for the Fc portion of IgG, to the immunologic response to antigen has not been assessed in health or disease. We examined the role of T gamma cells in antigen-induced blastogenesis of T cells from healthy subjects and characterized their participation in monocyte- and prostaglandin-mediated suppression. Cell fractions enriched in the depleted of T gamma cells were prepared from nonadherent T cells by preparative rosetting with IgG-sensitized ox erythrocytes; antigen-induced blastogenesis was assayed as 3H-thymidine incorporation (3H-TdR), by microculture techniques. Removal of T gamma cells resulted in a Tnon gamma cell fraction whose in vitro response to soluble antigen was a mean 40% +/- 8 less than the response of the unseparated T cells from the same donors. Antigen did not induce 3H-TdR in cultures of T gamma cells; however, in cell-mixing experiments, addition of autologous T gamma cells reconstituted the antigen responsiveness of the Tnon gamma cell fraction. Monocytes (MN) added to cell cultures at a ratio known to be suppressive in vitro (MN to T = 1:4) significantly decreased antigen-induced 3H-TdR of unseparated T cells but did not alter the antigen responses of Tnon gamma cells. MN-dependent suppression was abrogated by co-culture with indomethacin. Exogenous prostaglandin E2, an immunosuppressive cyclooxygenase product of MN, selectively decreased antigen-induced 3H-TdR of cell cultures containing T gamma cells but did not affect antigen responses of Tnon gamma cell fraction. Thus these studies show that MN and their cyclooxygenase products modulate T gamma cells to function in a suppressive mode. This demonstration of divergent T gamma cell functions indicates that the contribution of an expanded T gamma cell population to altered antigen reactivity in disease can be determined only by careful functional studies.
D000328:Adult; D000941:Antigens / Q000276:immunology; D002450:Cell Communication; D015232:Dinoprostone; D005260:Female; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007700:Kinetics; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D011458:Prostaglandins E / Q000378:metabolism; D011961:Receptors, Fc; D017452:Receptors, IgG; D013299:Streptodornase and Streptokinase / Q000276:immunology; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology*; D014373:Tuberculin / Q000276:immunology
D000941:Antigens; D011458:Prostaglandins E; D011961:Receptors, Fc; D017452:Receptors, IgG; D014373:Tuberculin; D013299:Streptodornase and Streptokinase; D015232:Dinoprostone; D007213:Indomethacin