title: Human T cell leukemia/lymphoma virus-infected antigen-specific T cell clones: indiscriminant helper function and lymphokine production.
abstract: The ability of human T cell leukemia/lymphoma virus (HTLV)-I to alter the function of infected T lymphocytes was examined directly by investigating the properties of an antigen-specific T cell clone before and after transformation with HTLV-I. Following infection, the T4 antigen-specific clone manifested a tenfold increase in its surface interleukin 2 (IL 2) receptor (Tac) density and acquired the viral determinants p19, p24, and 4D12 not present in the uninfected clone. Prior to infection, the T cell clone responded to antigen stimulation in the presence of histocompatible antigen-presenting cells with proliferation and secretion of multiple lymphokines, including IL 2, B cell growth factor (BCGF), B cell differentiation factor (BCDF), and interferon-gamma (IFN-gamma). Following infection, the T cell clone both proliferated and produced constitutively three of these lymphokines (BCGF, BCDF, and IFN-gamma) in the absence of accessory cells or antigen. Co-cultivation with any accessory cells regardless of histocompatibility resulted in increased proliferation and lymphokine production. IL 2 production by the HTLV-I-transformed cell, however, could not be detected. Similarly, the uninfected clone was able to provide B cell help for Ig production only when stimulated with both histocompatible cells and antigen. In contrast, the infected cell provided T cell help to B cells in an unregulated manner, independent of antigen or histocompatibility. Thus, functions such as the induction of proliferation, B cell help, and lymphokine production, which are finely regulated in uninfected antigen-specific T cell clones, became indiscriminant after HTLV-I infection.
authors.forename: D J
authors.initials: DJ
authors.lastname: Volkman
authors.forename: M
authors.initials: M
authors.lastname: Popovic
authors.forename: R C
authors.initials: RC
authors.lastname: Gallo
authors.forename: A S
authors.initials: AS
authors.lastname: Fauci
mesh_terms: D000956:Antigens, Viral / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology; D002454:Cell Differentiation; D002999:Clone Cells / Q000276:immunology; D017977:Deltaretrovirus / Q000276:immunology; D000939:Epitopes / Q000276:immunology; D006133:Growth Substances / Q000096:biosynthesis / Q000502:physiology; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D015847:Interleukin-4; D007938:Leukemia / Q000276:immunology*; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000096:biosynthesis* / Q000378:metabolism / Q000502:physiology; D011971:Receptors, Immunologic / Q000032:analysis; D015375:Receptors, Interleukin-2; D012192:Retroviridae Infections / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism
chemical_list: D000956:Antigens, Viral; D000939:Epitopes; D006133:Growth Substances; D007376:Interleukin-2; D008222:Lymphokines; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D015847:Interleukin-4; D007371:Interferon-gamma