The mechanism of retrovirus suppression of human T cell proliferation in vitro.
Immunosuppression is commonly associated with retrovirus-induced animal tumors. Studies in the murine and feline retrovirus systems suggest that the 15,000-dalton envelope protein (p15E) of the virion may contribute to immunosuppression by interfering with normal lymphocyte function. We examined the effect of inactivated feline leukemia virus (UV-FeLV) and p15E derived from this virus on concanavalin A (Con A) driven human T cell proliferation. Virus and p15E markedly suppressed mononuclear cell proliferative response to Con A. Suppression was not due to inhibition of monocyte accessory cell function, or interleukin 1 (IL 1) secretion. In fact, the presence of monocytes partially protected T cells from UV-FeLV suppression. UV-FeLV, however, suppressed T cell secretion of and response to interleukin 2 (IL 2). We conclude that UV-FeLV and derived p15E inhibit T cell proliferation by direct inhibition of T cell function. These findings, extended to the in vivo situations, suggest that retrovirus-associated suppression of the immune response involves the induction of T cell but not monocyte dysfunction.
D000328:Adult; D000818:Animals; D002415:Cats; D006801:Humans; D007165:Immunosuppression Therapy; D007375:Interleukin-1 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D005256:Leukemia Virus, Feline / Q000276:immunology / Q000528:radiation effects; D007942:Leukemia, Experimental / Q000276:immunology; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D009000:Monocytes / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014759:Viral Envelope Proteins / Q000276:immunology*
D007375:Interleukin-1; D007376:Interleukin-2; D014759:Viral Envelope Proteins