Mechanisms of T-cell functional deficiency in the acquired immunodeficiency syndrome.
Cell-mediated immune responses to cytomegalovirus infections were studied to define mechanisms for deficient effector T-cell responses in patients with the acquired immunodeficiency syndrome (AIDS). Progressive cytomegalovirus infection is common in such patients and is accompanied by a failure to develop HLA-restricted cytotoxic T-cell responses. The mechanism for the cytotoxic T-cell deficiency is presumably the basis for susceptibility to opportunistic infections. Precursors to these effector cells circulate in the peripheral blood of patients, but maturation of these cells into cytotoxic T cells is arrested during an interleukin-2-dependent phase. Production of interleukin-2 by lymphocytes from patients with AIDS is deficient because sera from these patients contain an inhibitor of interleukin-2 production. Excess suppressor cell activity does not appear to account for this deficient production. Studies of the source of the serum inhibitor should provide insights into the pathogenesis of AIDS and possible leads for effective treatment.
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007376:Interleukin-2 / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology; D008222:Lymphokines / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D007376:Interleukin-2; D008222:Lymphokines