Document 0694 DOCN M9440694 TI Proliferative response of CD4+ and CD8+ T cell subsets from Hispanics with HIV+ and AIDS: the superantigen hypothesis. DT 9404 AU Eylar EH; Rivera-Quinones C; Laroche HI; Yamamura Y; Ponce School of Medicine, Department of Biochemistry, Puerto; Rico. SO J Acquir Immune Defic Syndr. 1994 Feb;7(2):124-8. Unique Identifier : AIDSLINE MED/94133080 AB It has been hypothesized that the progressive deletion of CD4+ T cells in the course of infection due to human immunodeficiency virus (HIV) may be mediated in part by interaction with a superantigen inherent in an HIV protein. Consequently, selective loss of CD4+ cells with a T cell receptor V beta-chain capable of interaction with superantigen would produce a CD4+ population less or totally unresponsive to superantigen such as staphylococcal enterotoxins B and A (SEB and SEA respectively), but not to other mitogens such as concanavalin A, anti-CD3 (OKT3), or pokeweed mitogen. We tested this hypothesis by comparing the proliferative response of SEB and SEA with the other mitogens for 25 controls, 20 HIV+, and 15 donors with acquired immune deficiency syndrome (AIDS). We found that peripheral blood mononuclear cells, as well as the CD4+ and CD8+ subsets from both HIV+ and AIDS sources, the degree of suppression of mitogenesis for SEB and SEA was approximately equal to or less than that of the other mitogens. Moreover, suppression of HIV+ CD4+ and CD8+ T cell responses to SEB and SEA was equal (26%). If HIV superantigens exist, our data suggest that they are not responsible for the selective depletion of the CD4+ T cell subset as evaluated by SEB and SEA specificity. DE Acquired Immunodeficiency Syndrome/*IMMUNOLOGY Adolescence Adult Antigens, CD8/ANALYSIS Child Enterotoxins/IMMUNOLOGY Human HIV Antigens/IMMUNOLOGY HIV Seropositivity/*IMMUNOLOGY Lymphocyte Transformation Puerto Rico Staphylococcus aureus/IMMUNOLOGY Superantigens/*IMMUNOLOGY Support, U.S. Gov't, P.H.S. T-Lymphocytes, Suppressor-Effector/*IMMUNOLOGY T4 Lymphocytes/*IMMUNOLOGY JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).