Document 0141 DOCN M9460141 TI The interleukin-2 receptor subunit expression and function on peripheral blood lymphocytes from HIV-infected and control persons. DT 9404 AU Vanham G; Kestens L; Vingerhoets J; Penne G; Colebunders R; Vandenbruaene M; Goeman J; Ceuppens JL; Sugamura K; Gigase P; Institute of Tropical Medicine, Antwerp, Belgium. SO Clin Immunol Immunopathol. 1994 Apr;71(1):60-8. Unique Identifier : AIDSLINE MED/94185340 AB The expression of interleukin-2 receptor (IL2R) was studied on circulating lymphocytes from HIV-infected (HIV+) and control subjects, using chain-specific monoclonal antibodies and indirect immunofluorescence flow cytometry. The IL2R alpha chain expression was decreased on CD4 and CD8 T cells from HIV+ persons compared to controls. Conversely, beta chain expression was enhanced on both T cell subsets from the patients. IL2R-subunit levels were similar on natural killer cells from patients and controls. To evaluate the function of IL2R, we investigated to what extent IL2 could induce CD69, an early activation marker of lymphocytes. A dose-dependent increase of CD69 expression was observed on T and NK cells from all subjects. The upregulation of CD69 was similar on CD4 T and NK cells from patients and controls, but was more pronounced on CD8 T cells from HIV+ compared to HIV- subjects. Based on inhibition studies, both the alpha and the beta chain contributed to the IL-2-induced CD69 expression on CD4 T cells, pointing to involvement of the high-affinity receptor. The early activation of CD8 T cells and NK cells was mainly dependent on the intermediate-affinity receptor. We conclude that significant changes in IL2R alpha and beta chain expression on circulating T cells occur after HIV infection, but that early activation through IL2 is preserved or enhanced, even in advanced stages. DE Adult Antigens, CD/PHYSIOLOGY Antigens, Differentiation, T-Lymphocyte/PHYSIOLOGY Human HIV Infections/METABOLISM/*PATHOLOGY HIV Seronegativity/PHYSIOLOGY HIV Seropositivity/METABOLISM/PHYSIOPATHOLOGY Receptors, Antigen, T-Cell, alpha-beta/ANTAGONISTS & INHIB/ PHYSIOLOGY Receptors, Interleukin-2/*PHYSIOLOGY Support, Non-U.S. Gov't Up-Regulation (Physiology)/DRUG EFFECTS JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).