Abstract:
Antigen activation of T cells stimulates the de novo synthesis and secretion of interleukin-2 (IL-2 or T-cell growth factor) and the expression of high and low affinity IL-2 receptors. The interaction of IL-2 with its high affinity receptor stimulates cellular proliferation, producing an expansion of the antigen-reactive clonal T-cell population. The activation process culminates in the generation of specific effector cells mediating helper, suppressor, and cytotoxic T-cell functions. Study of the human IL-2 receptor has been aided by the identification of a monoclonal antireceptor antibody, termed anti-Tac. Deregulated IL-2 receptor expression in T cells infected with the human T lymphotropic virus types I and II (HTLV-I and HTLV-II) has been detected. Salient features of IL-2 receptor expression in normal and neoplastic T cells are presented. The human IL-2 receptor (Tac) has been characterized at the protein, mRNA, and gene levels. The receptor protein is a glycosylated, sulfated, and phosphorylated 55,000-dalton transmembrane structure that contains a very short cytoplasmic tail. There are multiple IL-2 receptor (Tac) mRNAs within activated T cells. The protein sequence of the IL-2 receptor has been determined by analysis of a full-length IL-2 receptor cDNA. The receptor is composed of 272 amino acids, including a 21-residue signal peptide. The IL-2 receptor gene has been isolated and shown to be organized within 8 exons and 7 introns. In situ hybridization studies have localized this receptor gene to chromosome 10p band 14----15. Deregulated expression of IL-2 receptors has been detected in T-cell lines transformed with the oncogenic HTLV-I retrovirus. The constitutive expression of IL-2 receptors in adult T-cell leukemia (ATL) cell lines has been studied in considerable detail. ATL cell lines constitutively express large quantities of IL-2 receptor mRNA and each of the three known poly A addition sites are utilized. Cotransfection studies have demonstrated that the tat-I gene product is able to fully activate the human IL-2 receptor promoter and partially activate the human IL-2 promoter. These findings suggest the possibility that the tat-I-induced changes in these cellular genes that normally regulate T cell growth may play a role in HTLV-I-induced T-cell transformation. (33 Refs)
Keywords: Gene Expression Regulation Human HTLV-BLV Infections/*IMMUNOLOGY Leukemia/*IMMUNOLOGY Receptors, Immunologic/ANALYSIS/*GENETICS RNA, Messenger/ANALYSIS T-Lymphocytes/*IMMUNOLOGY JOURNAL ARTICLE
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