Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3 - Wikidata - awgldk - TriplyDB

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

http://www.wikidata.org/entity/Q36742247

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DOCK8 deficiency impairs CD8 T cell survival and function in humans and mice Modulation of autoimmune diseases by interleukin (IL)-17 producing regulatory T helper (Th17) cells Transcription factor IRF8 directs a silencing programme for TH17 cell differentiation Genomic views of STAT function in CD4+ T helper cell differentiation Circulating Th17, Th22, and Th1 cells are increased in psoriasis A homozygous CARD9 mutation in a family with susceptibility to fungal infections Secukinumab for rheumatology: development and its potential place in therapy A Central Role for STAT3 in Gammaherpesvirus-Life Cycle and -Diseases The Innate Immune System in Acute and Chronic Wounds Immunity to Pathogens Taught by Specialized Human Dendritic Cell Subsets STATs: An Old Story, Yet Mesmerizing Interleukin 17-Mediated Host Defense against Candida albicans Inborn errors of human STAT1: allelic heterogeneity governs the diversity of immunological and infectious phenotypes Where does a Staphylococcus aureus vaccine stand?IL-23/IL-17A Dysfunction Phenotypes Inform Possible Clinical Effects from Anti-IL-17A Therapies T-regulatory cells in primary immune deficiencies Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity Hyper-IgE syndrome update Defining the functional states of Th17 cells Oropharyngeal Candidiasis in HIV Infection: Analysis of Impaired Mucosal Immune Response to Candida albicans in Mice Expressing the HIV-1 Transgene Covering all the Bases: Preclinical Development of an Effective Staphylococcus aureus Vaccine Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy Development of a vaccine against Staphylococcus aureus An update on the hyper-IgE syndromes Regulatory T-cells: diverse phenotypes integral to immune homeostasis and suppression Th17 effector cells support B cell responses outside of germinal centres The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing Mechanisms underlying helper T-cell plasticity: implications for immune-mediated disease.Cancers Related to Immunodeficiencies: Update and Perspectives Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis T(H)17 cells promote microbial killing and innate immune sensing of DNA via interleukin 26 Human TYK2 deficiency: Mycobacterial and viral infections without hyper-IgE syndrome Review of ustekinumab, an interleukin-12 and interleukin-23 inhibitor used for the treatment of plaque psoriasis Clinical manifestations, etiology, and pathogenesis of the hyper-IgE syndromes HIV and Tuberculosis: a Deadly Human Syndemic Key role of water-insoluble allergens of pollen cytoplasmic granules in biased allergic response in a rat model Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines.T- and B-cell-mediated protection induced by novel, live attenuated pertussis vaccine in mice. Cross protection against parapertussis.A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3.Aspergillus and Fusarium corneal infections are regulated by Th17 cells and IL-17-producing neutrophils.

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P2860

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

http://www.wikidata.org/entity/Q36742247

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@ast

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@en

type

label

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@ast

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@en

prefLabel

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@ast

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@en

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Journal of Experimental Medicine

P1476

Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3

@en

P2093

Archana Priyadarshi

http://www.w3.org/2001/XMLSchema#string

Bodo Grimbacher

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David A Fulcher

http://www.w3.org/2001/XMLSchema#string

Gary Y J Chew

http://www.w3.org/2001/XMLSchema#string

Matthew C Cook

http://www.w3.org/2001/XMLSchema#string

Melanie Wong

http://www.w3.org/2001/XMLSchema#string

Nicholas Simpson

http://www.w3.org/2001/XMLSchema#string

P2860

A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rbeta1 and a novel cytokine receptor subunit, IL-23R

Mutations in TWIST, a basic helix-loop-helix transcription factor, in Saethre-Chotzen syndrome

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells

Transforming growth factor-beta induces development of the T(H)17 lineage

STAT3 mutations in the hyper-IgE syndrome

IL-22 increases the innate immunity of tissues

STAT3 regulates cytokine-mediated generation of inflammatory helper T cells

TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells

Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome

Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation

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5260930

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18591410

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2442632

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