Epstein-Barr virus increases the proliferative response and the generation of suppressor and cytotoxic T-cell functions in autologous mixed lymphocyte reaction.
Epstein-Barr virus (EBV) infection of stimulator cells significantly increased the proliferative response of T cells in the autologous mixed lymphocyte reaction (AMLR). The addition of a monoclonal anti-HLA-DR antibody to AMLR cultures in which either EBV-infected or non-infected non-T cells were used as stimulator cells strongly inhibited the proliferative response irrespective of the presence of EBV. It is concluded that EBV does not by itself activate the responding cells and that HLA-DR antigens are necessary to trigger T cells. Increased generation of suppressor T cells, determined in both alloantigen-induced DNA synthesis and pokeweed-mitogen-stimulated immunoglobulin production, was found after an EBV infection of stimulator cells. Similarly, EBV-infected non-T cells significantly increased the generation of killer T cells, determined in three different types of target cells: phytohaemagglutinin-stimulated mononuclear cells, EBV-transformed cells, and concanavalin-A-activated murine spleen cells. The increased T-cell responses after an EBV infection may reflect the attempts in vivo to control and hold in check the viral infection.
D000911:Antibodies, Monoclonal / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis; D003602:Cytotoxicity, Immunologic; D004854:Herpesvirus 4, Human; D006801:Humans; D007244:Infectious Mononucleosis / Q000209:etiology / Q000276:immunology*; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D013601:T-Lymphocytes / Q000276:immunology* / Q000382:microbiology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D000911:Antibodies, Monoclonal; D001323:Autoantibodies