title: [Up-to-date findings in the host defence mechanism to cryptococcus infection].
abstract: Cryptococcus neoformans is a medically important opportunistic fungal pathogen with a polysaccharide capsule surrounding the yeast-like cells. In hosts with impaired cell-mediated immunity such as AIDS, uncontrolled infection causes life-threatening meningoencephalitis. In immunocompetent individuals, the host immune response usually limits the growth of the fungal pathogen at the primary infected site, where it may persist, without completely eradicated, in a latent state because of its ability to escape from killing by macrophages. Th1 response in adaptive immunity is essential for the host defense to cryptococcal infection, in which interferon (IFN)-γ polarizes innate macrophages into fungicidal M1 macrophages. Recently, we found that caspase recruitment domain family member (CARD9), an adaptor protein in a signal transduction triggered by C-type lectin receptors, plays a key role in the early production of IFN-γ at the site of infection by recruiting NK cells and CD4(+) and CD8(+) memory-phenotype T cells. We also found that IL-4 produced by Th2 cells stimulates broncoepithelial cells to secrete mucin, which may lead to promotion in the mucociliary clearance of C. neoformans. Here, we summarize the up-to-date findings in the host defense mechanism to this infection with focusing on our recent data.
authors.affiliation: Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine.
authors.forename: Keiko
authors.initials: K
authors.lastname: Ishii
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Kawakami
mesh_terms: D001980:Bronchi / Q000166:cytology / Q000378:metabolism; D053468:CARD Signaling Adaptor Proteins / Q000502:physiology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D003453:Cryptococcosis / Q000276:immunology* / Q000382:microbiology*; D003455:Cryptococcus neoformans / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity; D004847:Epithelial Cells / Q000378:metabolism; D006801:Humans; D007111:Immunity, Cellular; D007121:Immunocompetence / Q000276:immunology; D016867:Immunocompromised Host / Q000276:immunology; D007371:Interferon-gamma / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type / Q000502:physiology; D008264:Macrophages / Q000276:immunology; D009077:Mucins / Q000378:metabolism; D009079:Mucociliary Clearance / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D053468:CARD Signaling Adaptor Proteins; C505855:CARD9 protein, human; D037181:Lectins, C-Type; D009077:Mucins; D015847:Interleukin-4; D007371:Interferon-gamma