title: Sera from patients with the acquired immunodeficiency syndrome inhibit production of interleukin-2 by normal lymphocytes.
abstract: We studied the effects of sera from patients with the acquired immunodeficiency syndrome (AIDS) on interleukin-2 (IL-2) production to help elucidate the mechanism of immunodeficiency. Compared with sera from healthy controls, sera from AIDS patients suppressed phytohemagglutinin (PHA)-induced IL-2 production by normal blood mononuclear cells. Sera from homosexual contacts of AIDS patients and from adults with acute cytomegalovirus infection generally lacked this suppressive activity. The effect of the AIDS sera could not be attributed to absence of a stimulatory or nutritive factor, to inactivation of IL-2, to inhibition of the IL-2 assay, nor to increased turnover of IL-2. The suppressive effect of the sera was not mediated by radiosensitive or T8 antigen-bearing suppressor cells or by increased prostaglandin production or decreased interleukin-1 production. The sera acted directly on the groups of cells that produce IL-2, T cells and large granular lymphocytes; suppression occurred at an early, probably pretranslational, stage. When cells were incubated with AIDS sera and then washed, the suppressive effect persisted. The sera did not cause direct or complement-mediated cytotoxic effects on normal mononuclear cells nor did they suppress PHA-induced interferon production, nor proliferation of T lymphoblasts or lymphocyte lines. The suppressive effect was not mediated by interferon, cortisol, immunoglobulin G or M, or immune complexes. The activity was stable at pH 3, pH 10, and 60 degrees C; inactivated at 100 degrees C; and not ether extractable. Because IL-2 plays a central role in the development of many immune responses, the serum factor(s) that inhibits IL-2 production could contribute significantly to the immunodeficiency of AIDS.
authors.forename: J P
authors.initials: JP
authors.lastname: Siegel
authors.forename: J Y
authors.initials: JY
authors.lastname: Djeu
authors.forename: N I
authors.initials: NI
authors.lastname: Stocks
authors.forename: H
authors.initials: H
authors.lastname: Masur
authors.forename: E P
authors.initials: EP
authors.lastname: Gelmann
authors.forename: G V
authors.initials: GV
authors.lastname: Quinnan
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000097:blood / Q000276:immunology*; D002478:Cells, Cultured; D003586:Cytomegalovirus Infections / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D007213:Indomethacin / Q000494:pharmacology; D007376:Interleukin-2 / Q000096:biosynthesis*; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D011971:Receptors, Immunologic / Q000276:immunology; D015375:Receptors, Interleukin-2; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D007213:Indomethacin