| 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. |
