title: Increased Fas antigen expression in murine retrovirus-induced immunodeficiency syndrome, MAIDS.
abstract: The Fas antigen (Fas), which is a cell surface protein belonging to the tumor necrosis factor receptor family, mediates apoptosis. To assess the contribution of Fas to the pathogenesis of retrovirus-induced immunodeficiency, we examined the kinetics of Fas expression on the lymphocytes during the course of murine acquired immunodeficiency syndrome (MAIDS) induced by a defective LP-BM5 murine leukemia virus. The Fas-positive cells were increased in proportion both in alpha beta T cells and B cells with the progression of MAIDS. The appearance of Fas-positive cells in alpha beta T cells preceded those in B cells during the course of MAIDS. Among alpha beta T cells, about half of the Thy1.2+ alpha beta T cells were positive for Fas, while almost all of Thy1.2- CD4+ alpha beta T cells were of the Fas-positive phenotype. The Fas-positive cells in MAIDS mice, especially unique Thy1.2-CD4+ alpha beta T cells, were easily rendered apoptotic by stimulation via Fas, indicating that Fas expressed on the lymphocytes is functional. Furthermore, concomitant infection with Mycobacterium avium in MAIDS mice caused a marked increase in Fas-positive cells accompanied by a severely impaired T cell reactivity to polyclonal stimuli. Taken together, these results suggest that possible participation of the Fas system in the pathogenesis of retrovirus-induced immunodeficiency.
authors.affiliation: Laboratory of Germfree Life, Research Institute for Disease, Nagoya University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hiromatsu
authors.forename: Y
authors.initials: Y
authors.lastname: Aoki
authors.forename: M
authors.initials: M
authors.lastname: Makino
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Mizuochi
authors.forename: Y
authors.initials: Y
authors.lastname: Gotoh
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
authors.forename: J
authors.initials: J
authors.lastname: Ogasawara
authors.forename: S
authors.initials: S
authors.lastname: Nagata
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshikai
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000378:metabolism*; D017209:Apoptosis; D001402:B-Lymphocytes / Q000276:immunology*; D004249:DNA Damage; D005260:Female; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology*; D009162:Mycobacterium avium / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013997:Time Factors; D014376:Tuberculosis / Q000150:complications / Q000276:immunology; D019014:fas Receptor
chemical_list: D000954:Antigens, Surface; D016693:Receptors, Antigen, T-Cell, alpha-beta; D019014:fas Receptor