title: Both CD4+ and CD8+ lymphocytes reduce the severity of tissue lesions in murine systemic cadidiasis, and CD4+ cells also demonstrate strain-specific immunopathological effects.
abstract: The role of T lymphocytes in host responses to sublethal systemic infection with Candida albicans was evaluated by mAb depletion of CD4+ and CD8+ cells from BALB/c and CBA/CaH mice, which develop mild and severe tissue damage, respectively. Depletion of CD4+ lymphocytes from BALB/c mice markedly increased tissue damage, but did not alter the course of infection. In CBA/CaH mice, depletion of CD4+ cells abrogated tissue destruction in both brain and kidney at day 4 after infection, and significantly decreased fungal colonization in the brain. However, the severity of tissue lesions increased relative to controls from day 8 onwards. A small increase in tissue damage was evident in both mouse strains after depletion of CD8+ cells. There were no major differences between days 4 and 8 after infection in cDNA cytokine profiles of CD4+ lymphocytes from either BALB/c or CBA/CaH mice. After passive transfer into infected syngeneic recipients, spleen cells from infected CBA/CaH mice markedly increased tissue damage when compared to controls, and also caused a significant increase in fungal colonization in the brain. A similar transfer in BALB/c mice increased the number of inflammatory cells in and around the lesions, but had no effect on the fungal burden in brain and kidney. The data demonstrate that both CD4+ and CD8+ lymphocytes contribute to the reduction of tissue damage after systemic infection with C. albicans, and that the development and expression of CD4+ lymphocyte effector function is influenced by the genetic background of the mouse.
authors.affiliation: Pathology Department, University of Western Australia, Nedlands, WA 6009, Australia.|School of Dentistry, University of Queensland, Brisbane, Qld 4072, Australia.
authors.forename: Robert B
authors.initials: RB
authors.lastname: Ashman
authors.affiliation: Pathology Department, University of Western Australia, Nedlands, WA 6009, Australia.
authors.forename: Alma
authors.initials: A
authors.lastname: Fulurija
authors.affiliation: Pathology Department, University of Western Australia, Nedlands, WA 6009, Australia.
authors.forename: John M
authors.initials: JM
authors.lastname: Papadimitriou
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001921:Brain / Q000382:microbiology / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002176:Candida albicans / Q000276:immunology*; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D007668:Kidney / Q000382:microbiology / Q000473:pathology; D008212:Lymphocyte Depletion; D051379:Mice; D008807:Mice, Inbred BALB C; D008808:Mice, Inbred CBA; D013045:Species Specificity; D013154:Spleen / Q000166:cytology / Q000276:immunology
chemical_list: D016207:Cytokines