title: Functional alterations of herpes simplex virus-specific CD4+ multifunctional T cell clones following infection with human T lymphotropic virus type I.
abstract: In an attempt to understand the mechanisms of immunodeficiency induced by human T lymphotropic virus type I (HTLV-I), HSV-specific CD4+ human multifunctional T cell clones were infected with HTLV-I in vitro. Early after HTLV-I infection, when their growth was still IL-2-dependent, clones were found to have almost completely lost their cytotoxic activity. At that time, their HSV-Ag-induced proliferative response and helper function for anti-HSV antibody production by B cells were only partially impaired. After this initial phase, the HTLV-I-infected clone became IL-2-independent, and the helper function was also completely lost. IL-2-dependent HTLV-I-infected clones showed degrees of proliferative response and elevation of intracellular free Ca2+ concentration induced by anti-CD3 mAb equivalent to those of HTLV-I-uninfected clones. On the other hand, during the IL-2-independent stage, expression of CD3-TCR complex on the cell surface was markedly decreased, and no significant elevation of intracellular free Ca2+ concentration was detected in response to anti-CD3 mAb. These data indicated that the loss of cytotoxic activity of HSV-specific T cell clones observed early after HTLV-I infection was not the result of impaired antigen recognition via the CD3-TCR complex, but might be due to dysfunction in the effector phase. On the other hand, the dysfunction of helper activity found late after HTLV-I infection might have mainly occurred in the recognition phase due to the decreased expression of CD3-TCR complex. The present data appear to suggest certain aspects of the pathogenesis of the immunodeficiency occurring in HTLV-I infection.
authors: First Department of Internal Medicine, Ehime University School of Medicine, Japan.
authors: A
authors: A
authors: Inatsuki
authors: M
authors: M
authors: Yasukawa
authors: Y
authors: Y
authors: Kobayashi
mesh_terms: D000945:Antigens, Differentiation, T-Lymphocyte / Q000502:physiology; D000956:Antigens, Viral / Q000276:immunology*; D002999:Clone Cells / Q000145:classification / Q000276:immunology / Q000382:microbiology; D000939:Epitopes / Q000276:immunology; D015329:Gene Rearrangement, T-Lymphocyte; D015368:Human T-lymphotropic virus 1 / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation; D010641:Phenotype; D011533:Proviruses / Q000302:isolation & purification; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000502:physiology; D012191:Retroviridae Proteins / Q000302:isolation & purification; D015398:Signal Transduction; D018139:Simplexvirus / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000145:classification* / Q000276:immunology / Q000382:microbiology
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D000956:Antigens, Viral; D000939:Epitopes; D011948:Receptors, Antigen, T-Cell; D012191:Retroviridae Proteins