title: T cell subsets and IFN-gamma production in resistance to systemic candidosis in immunized mice.
abstract: In addition to previous evidence for the roles of T cell-dependent immunity and delayed-type hypersensitivity in acquired resistance to systemic candidosis in mice, in the present study we have investigated the relative contributions of L3T4+ and Lyt-2+ lymphocytes in the protective immunity induced by vaccination with low virulence Candida albicans cells. We have also addressed the issue of the mode of Candida Ag recognition by specific T cells leading to cytokine release. Spleen cells from immunized mice produced high levels of IFN-gamma in vitro in response to Candida Ag, and this activity was abolished only by the combined treatment of the responder population with anti-L3T4 and anti-Lyt-2.2 mAb plus C. Positively selected L3T4+ and Lyt-2+ cells also produced IFN-gamma in vitro, provided accessory cells (plastic-adherent and Thy-1- Ia- splenocytes, respectively) were added to the lymphocyte-yeast cell cocultures. The production of IFN-gamma by purified L3T4+ and Lyt-2+ cells was inhibited by addition of the respective anti-class II and anti-class I H-2 antibody to the cultures. In vivo, administration of anti-L3T4, anti-Lyt-2.2 mAb or a combination of both significantly impaired the resistance of immunized mice to challenge with virulent C. albicans, as manifested by increased recovery of the yeast from the mouse kidneys. A similar effect was observed upon neutralization of endogenous IFN-gamma by treatment with rat mAb. These results suggest that both L3T4+ and Lyt-2+ T cells play a role in acquired immunity to systemic C. albicans infection, and that their activity may involve IFN-gamma-mediated stimulation of candidacidal mechanisms.
authors.affiliation: Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Cenci
authors.forename: L
authors.initials: L
authors.lastname: Romani
authors.forename: A
authors.initials: A
authors.lastname: Vecchiarelli
authors.forename: P
authors.initials: P
authors.lastname: Puccetti
authors.forename: F
authors.initials: F
authors.lastname: Bistoni
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D000950:Antigens, Ly / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology; D005260:Female; D006183:H-2 Antigens / Q000502:physiology; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007111:Immunity, Cellular; D007114:Immunization; D066298:In Vitro Techniques; D007371:Interferon-gamma / Q000096:biosynthesis*; D007376:Interleukin-2 / Q000096:biosynthesis; D007668:Kidney / Q000382:microbiology; D008213:Lymphocyte Activation; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D000950:Antigens, Ly; D006183:H-2 Antigens; D007376:Interleukin-2; D007371:Interferon-gamma