ArticleInfection and immunity2010
Interleukin-17 is not required for classical macrophage activation in a pulmonary mouse model of Cryptococcus neoformans infection.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Peripheral blood CD4The Journal of infection · 2025Article
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- Innate phase production of IFN-γ by memory and effector T cells expressing early activation marker CD69 during infection withInfection and immunity · 2024Article
- Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023Review
- Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Vaccine protection by Cryptococcus neoformans Δsgl1 is mediated by γδ T cells via TLR2 signaling.Mucosal immunology · 2022Article
- Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs.Scientific reports · 2021Article
- Immune Sensing and Potential Immunotherapeutic Approaches to Control Chromoblastomycosis.Journal of fungi (Basel, Switzerland) · 2020Review
- Limited Role of Mincle in the Host Defense against Infection with Cryptococcus deneoformans.Infection and immunity · 2020Article
- Article
- Modulation of Wnt/β-catenin signaling in IL-17A-mediated macrophage polarization of RAW264.7 cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Group 2 Innate Lymphoid Cells (ILC2) Suppress Beneficial Type 1 Immune Responses During Pulmonary Cryptococcosis.Frontiers in immunology · 2020Article
- Lung-infiltrating T helper 17 cells as the major source of interleukin-17A production during pulmonary Cryptococcus neoformans infection.BMC immunology · 2018Article
- Article
- Innate Immunity against Cryptococcus, from Recognition to Elimination.Journal of fungi (Basel, Switzerland) · 2018Review
- Contribution of IL-1RI Signaling to Protection againstFrontiers in immunology · 2017Article
- Extracellular vesicles from Paracoccidioides brasiliensis induced M1 polarization in vitro.Scientific reports · 2016Article
- Antifungal Activity of Plasmacytoid Dendritic Cells against Cryptococcus neoformans In Vitro Requires Expression of Dectin-3 (CLEC4D) and Reactive Oxygen Species.Infection and immunity · 2016Article
- Innate host defenses against Cryptococcus neoformans.Journal of microbiology (Seoul, Korea) · 2016Review
- Article
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4 authors.
Funding
Abstract
Cryptococcus neoformans is an opportunistic fungal pathogen that causes disease in individuals with suppressed cell-mediated immunity. Recent studies in our laboratory have shown that increases in pulmonary Th1-type and interleukin-17A (IL-17A) cytokine production, classical macrophage activation, and sterilizing immunity are elicited in response to infection with a gamma interferon (IFN-γ)-producing C. neoformans strain, H99γ. IL-17A-treated macrophages, compared to IL-4-treated macrophages, have been demonstrated to exhibit increased microbicidal activity in vitro, a characteristic consistent with classical macrophage activation. The purpose of these studies is to determine the role of IL-17A in the induction of classically activated macrophages following infection with C. neoformans. Immunohistochemistry and real-time PCR were used to characterize the macrophage activation phenotype in lung tissues of mice treated with isotype control or anti-IL-17A antibodies and given an experimental pulmonary infection with C. neoformans strain H99γ. The pulmonary fungal burden was resolved, albeit more slowly, in mice depleted of IL-17A compared to the fungal burden in isotype control-treated mice. Nonetheless, no difference in classical macrophage activation was observed in IL-17A-depleted mice. Similarly, classical macrophage activation was evident in mice deficient in IL-17A or the IL-17 receptor A, which mediates IL-17A signaling, following pulmonary infection with wild-type C. neoformans strain H99 or H99γ. These studies suggest that IL-17A may play a role in the early immune response to C. neoformans but is not required for classical macrophage activation in mice experimentally infected with C. neoformans.
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