Role of IL-17A on resolution of pulmonary C. neoformans infection - Wikidata - awgldk - TriplyDB

Role of IL-17A on resolution of pulmonary C. neoformans infection

Role of IL-17A on resolution of pulmonary C. neoformans infection

http://www.wikidata.org/entity/Q33832023

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Cryptococcus-Related Immune Reconstitution Inflammatory Syndrome (IRIS): Pathogenesis and its Clinical Implications Cryptococcus and Phagocytes: Complex Interactions that Influence Disease Outcome Host immunity to Cryptococcus neoformans Elucidating the immunological function of the Cryptococcus neoformans capsule Adaptive immunity to fungi Endemic mycoses in patients with STAT3-mutated hyper-IgE (Job) syndrome Lack of IL-4 receptor expression on T helper cells reduces T helper 2 cell polyfunctionality and confers resistance in allergic bronchopulmonary mycosis Vaccine-mediated immune responses to experimental pulmonary Cryptococcus gattii infection in mice Scavenger receptor A modulates the immune response to pulmonary Cryptococcus neoformans infection.Characterization of IL-22 and antimicrobial peptide production in mice protected against pulmonary Cryptococcus neoformans infection.Immune modulation mediated by cryptococcal laccase promotes pulmonary growth and brain dissemination of virulent Cryptococcus neoformans in mice.Depletion of neutrophils in a protective model of pulmonary cryptococcosis results in increased IL-17A production by γδ T cells.IL-17A impairs host tolerance during airway chronic infection by Pseudomonas aeruginosa Dectin-2 deficiency promotes Th2 response and mucin production in the lungs after pulmonary infection with Cryptococcus neoformans.Binding of the wheat germ lectin to Cryptococcus neoformans chitooligomers affects multiple mechanisms required for fungal pathogenesis.Adaptive immunity to fungi.Cytokine profiles at admission can be related to outcome in AIDS patients with cryptococcal meningitis Cerebrospinal fluid cytokine profiles predict risk of early mortality and immune reconstitution inflammatory syndrome in HIV-associated cryptococcal meningitis Contributions of the MyD88-dependent receptors IL-18R, IL-1R, and TLR9 to host defenses following pulmonary challenge with Cryptococcus neoformans.Paradoxical Immune Responses in Non-HIV Cryptococcal Meningitis Type I IFN Induction via Poly-ICLC Protects Mice against Cryptococcosis.Cryptococcus neoformans Infection in Mice Lacking Type I Interferon Signaling Leads to Increased Fungal Clearance and IL-4-Dependent Mucin Production in the Lungs.IL-23 dampens the allergic response to Cryptococcus neoformans through IL-17-independent and -dependent mechanisms.Fonsecaea pedrosoi-induced Th17-cell differentiation in mice is fostered by Dectin-2 and suppressed by Mincle recognition Development of protective inflammation and cell-mediated immunity against Cryptococcus neoformans after exposure to hyphal mutants.Vaccine and immunotherapeutic approaches for the prevention of cryptococcosis: lessons learned from animal models.Vaccine-induced th17 cells are maintained long-term postvaccination as a distinct and phenotypically stable memory subset.Cryptococcus neoformans growth and protection from innate immunity are dependent on expression of a virulence-associated DEAD-box protein, Vad1.The phenotype of the Cryptococcus-specific CD4+ memory T-cell response is associated with disease severity and outcome in HIV-associated cryptococcal meningitis.X-linked immunodeficient mice exhibit enhanced susceptibility to Cryptococcus neoformans Infection.Immunity to infection in IL-17-deficient mice and humans Statins reduce spirochetal burden and modulate immune responses in the C3H/HeN mouse model of Lyme disease.Identification and characterization of Cryptococcus neoformans protein fractions that induce protective immune responses Interleukin-17A enhances host defense against cryptococcal lung infection through effects mediated by leukocyte recruitment, activation, and gamma interferon production Macrophage Cryptococcus interactions: an update.Type-I interferon secretion in the acute phase promotes Cryptococcus neoformans infection-induced Th17 cell polarization in vitro.Defect of CARD9 leads to impaired accumulation of gamma interferon-producing memory phenotype T cells in lungs and increased susceptibility to pulmonary infection with Cryptococcus neoformans.Cytokines and the regulation of fungus-specific CD4 T cell differentiation.Induction of protective immunity against cryptococcosis.Dysregulation in lung immunity - the protective and pathologic Th17 response in infection.

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Role of IL-17A on resolution of pulmonary C. neoformans infection

http://www.wikidata.org/entity/Q33832023

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年學術文章

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Role of IL-17A on resolution of pulmonary C. neoformans infection

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Floyd L Wormley

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Jay K Kolls

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Sarah E Hardison

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P2860

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

IL-17 and Th17 Cells

IL-17A-producing neutrophil-regulatory Tn lymphocytes

IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells

Cryptococcosis in the era of AIDS--100 years after the discovery of Cryptococcus neoformans.

IL-17A inhibits the expansion of IL-17A-producing T cells in mice through "short-loop" inhibition via IL-17 receptor.

Pertussis toxin stimulates IL-17 production in response to Bordetella pertussis infection in mice.

CD4+ T cells mediate abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism.

Insights into the mechanisms of protective immunity against Cryptococcus neoformans infection using a mouse model of pulmonary cryptococcosis

Pulmonary infection with an interferon-gamma-producing Cryptococcus neoformans strain results in classical macrophage activation and protection.

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Karen L. Wozniak

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