Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis. - Wikidata - wikimedia - TriplyDB

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

http://www.wikidata.org/entity/Q33577398

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Systems Level Dissection of Candida Recognition by Dectins: A Matter of Fungal Morphology and Site of Infection Niche-specific requirement for hyphal wall protein 1 in virulence of Candida albicans Differential adaptation of Candida albicans in vivo modulates immune recognition by dectin-1 IL-22 and IDO1 affect immunity and tolerance to murine and human vaginal candidiasis The WNT signaling pathway contributes to dectin-1-dependent inhibition of Toll-like receptor-induced inflammatory signature Decidual stromal cells recruit Th17 cells into decidua to promote proliferation and invasion of human trophoblast cells by secreting IL-17 Animal models for candidiasis Candida albicans commensalism in the gastrointestinal tract.Role of innate immune receptors in paradoxical caspofungin activity in vivo in preclinical aspergillosis.Dectin-1 is not required for controlling Candida albicans colonization of the gastrointestinal tract.Dectin-1 is required for resistance to coccidioidomycosis in mice.The game theory of Candida albicans colonization dynamics reveals host status-responsive gene expression.Dectin-1 activation controls maturation of β-1,3-glucan-containing phagosomes Tracing conidial fate and measuring host cell antifungal activity using a reporter of microbial viability in the lung The aryl hydrocarbon receptor in innate T cell immunity.Murine models of Candida gastrointestinal colonization and dissemination.Caspases as the key effectors of inflammatory responses against bacterial infection.The adaptor CARD9 is required for adaptive but not innate immunity to oral mucosal Candida albicans infections.Beyond Candida albicans: Mechanisms of immunity to non-albicans Candida species Contribution of TLR2 pathway in the pathogenesis of vulvovaginal candidiasis.Dexamethasone induced inhibition of Dectin-1 activation of antigen presenting cells is mediated via STAT-3 and NF-κB signaling pathways.The vaginal microbiota, host defence and reproductive physiology.Neutrophils influx and proinflammatory cytokines inhibition by sodium salicylate, unlike aspirin, in Candida albicans-induced peritonitis model.TLR-4 cooperates with Dectin-1 and mannose receptor to expand Th17 and Tc17 cells induced by Paracoccidioides brasiliensis stimulated dendritic cells.Dectin-1 Exerts Dual Control in the Gut.Dectin-1 induces M1 macrophages and prominent expansion of CD8+IL-17+ cells in pulmonary Paracoccidioidomycosis.Contribution of CARD9-mediated signalling to wound healing in skin.Dectin-1 Positive Dendritic Cells Expand after Infection with Leishmania major Parasites and Represent Promising Targets for Vaccine Development.Dectin-1/2-induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses.Hypoxia Promotes Immune Evasion by Triggering β-Glucan Masking on the Candida albicans Cell Surface via Mitochondrial and cAMP-Protein Kinase A Signaling Role of Short Chain Fatty Acids in Controlling T and Immunopathology During Mucosal Infection

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P2860

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

http://www.wikidata.org/entity/Q33577398

description

2012 nî lūn-bûn

@nan

2012 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի ապրիլին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

@zh-mo

2012年論文

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2012年论文

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name

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@ast

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@en

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@nl

type

label

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@ast

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@en

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@nl

prefLabel

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@ast

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@en

Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@nl

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Cellular and Molecular Immunology

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Dectin-1 isoforms contribute to distinct Th1/Th17 cell activation in mucosal candidiasis.

@en

P2093

Andrea Casagrande

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Carmen D'Angelo

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Giovanni Ricci

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Gloria Giovannini

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Rossana G Iannitti

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P2860

Human dectin-1 deficiency and mucocutaneous fungal infections

The beta-glucan receptor, dectin-1, is predominantly expressed on the surface of cells of the monocyte/macrophage and neutrophil lineages

The role of Dectin-1 in the host defence against fungal infections

Dectin-2 recognition of alpha-mannans and induction of Th17 cell differentiation is essential for host defense against Candida albicans

Syk-dependent cytokine induction by Dectin-1 reveals a novel pattern recognition pathway for C type lectins

Stage-specific sampling by pattern recognition receptors during Candida albicans phagocytosis.

PPARγ controls Dectin-1 expression required for host antifungal defense against Candida albicans.

Human dendritic cells activated via dectin-1 are efficient at priming Th17, cytotoxic CD8 T and B cell responses

Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity.

Epithelial cell-derived S100 calcium-binding proteins as key mediators in the hallmark acute neutrophil response during Candida vaginitis.

P2888

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276-286

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scholarly article

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10.1038/CMI.2012.1

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3

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9

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Agostinho Carvalho

Antonella De Luca

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2012-04-30T00:00:00Z

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224867569

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1050148689

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22543832

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4012853

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