title: Abnormal expression of IL-2R beta (p70)-binding polypeptide on HIV-infected patients' cells.
abstract: The constitutively expressed IL-2R beta (p70) chain participates in the formation of high-affinity (h.a.) IL-2R and transduces IL-2-mediated signals to normal cells. Its expression on HIV-infected patients' PBMC was evaluated and was found to be decreased in both nonstimulated CD4+ and CD8+ cells. Mitogenic cell stimulation induced IL-2R beta chain expression on both CD4+ and CD8+ cells from asymptomatic and persistent generalized lymphadenopathy patients but not on those from AIDS patients. Comparison of mean fluorescence intensity of IL-2R beta positively stained cells from normals and patients did not reveal significant differences. Cross-linking of 125I-rIL-2 on patients' PHA-blasts revealed decreased signals corresponding to both IL-2-binding chains and, in some cases, neither IL-2R alpha nor IL-2R beta chains could be detected. Decreased expression of IL-2R beta polypeptide was associated with impaired accumulation of the corresponding mRNA transcripts. Binding experiments with 125I-rIL-2 under h.a. conditions showed a decreased number of IL-2-binding sites/cell which was more pronounced in patients with AIDS than in patients with less advanced clinical stages. In vitro HIV infection of normal PHA-blasts also resulted in a decreased number of h.a. IL-2R/cell. High concentrations of rIL-2 in the absence of other mitogenic stimuli induced a decreased cell proliferation and expression of the IL-2R alpha chain and did not enhance the constitutive NK and the generation of LAK activity in several patients, suggesting an impaired IL-2R beta chain-mediated cell activation.
authors.affiliation: Oncogénèse Appliquée, INSERM U268, Hôpital Paul Brousse, Villejuif, France.
authors.forename: Y
authors.initials: Y
authors.lastname: Sahraoui
authors.forename: A
authors.initials: A
authors.lastname: Ammar
authors.forename: Y
authors.initials: Y
authors.lastname: Lunardi-Iskandar
authors.forename: A
authors.initials: A
authors.lastname: Tsapis
authors.forename: E
authors.initials: E
authors.lastname: Spanakis
authors.forename: N
authors.initials: N
authors.lastname: N'Go
authors.forename: M
authors.initials: M
authors.lastname: Allouche
authors.forename: V G
authors.initials: VG
authors.lastname: Bellile
authors.forename: C
authors.initials: C
authors.lastname: Jasmin
authors.forename: V
authors.initials: V
authors.lastname: Georgoulias
mesh_terms: D000911:Antibodies, Monoclonal; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D005786:Gene Expression Regulation / Q000276:immunology; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis / Q000037:antagonists & inhibitors; D015375:Receptors, Interleukin-2 / Q000037:antagonists & inhibitors / Q000276:immunology*; D011994:Recombinant Proteins / Q000494:pharmacology; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D015704:CD4 Antigens; D016827:CD8 Antigens; D007376:Interleukin-2; D012333:RNA, Messenger; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins