Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome - Wikidata - wikimedia - TriplyDB

Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome

Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome

http://www.wikidata.org/entity/Q37273205

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Genomic views of STAT function in CD4+ T helper cell differentiation Mitochondrial Stat3, the Need for Design Thinking RNase 7 in Cutaneous Defense Inborn errors of human STAT1: allelic heterogeneity governs the diversity of immunological and infectious phenotypes Where does a Staphylococcus aureus vaccine stand?STAT3 and the Hyper-IgE syndrome: Clinical presentation, genetic origin, pathogenesis, novel findings and remaining uncertainties Hyper-IgE syndrome update Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy An update on the hyper-IgE syndromes Mendelian genetics of human susceptibility to fungal infection Pathogenesis of Staphylococcus aureus abscesses The immunology of influenza virus-associated bacterial pneumonia The Hyper-IgE Syndromes: Lessons in Nature, From Bench to Bedside Innate Stat3-mediated induction of the antimicrobial protein Reg3γ is required for host defense against MRSA pneumonia Cooperative interactions between TLR4 and TLR9 regulate interleukin 23 and 17 production in a murine model of gram negative bacterial pneumonia.A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3.B cell-intrinsic signaling through IL-21 receptor and STAT3 is required for establishing long-lived antibody responses in humans.Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I Molecular Typing of Staphylococcus aureus Isolated from Patients with Autosomal Dominant Hyper IgE Syndrome.Invasive fungal disease in autosomal-dominant hyper-IgE syndrome.Primary immunodeficiencies underlying fungal infections Intermediate phenotypes in patients with autosomal dominant hyper-IgE syndrome caused by somatic mosaicism.Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity.Autoimmunity, hypogammaglobulinemia, lymphoproliferation, and mycobacterial disease in patients with activating mutations in STAT3.Defective IL-10 signaling in hyper-IgE syndrome results in impaired generation of tolerogenic dendritic cells and induced regulatory T cells.IL-17A and IFN-γ synergistically induce RNase 7 expression via STAT3 in primary keratinocytes Influenza A inhibits Th17-mediated host defense against bacterial pneumonia in mice Mechanisms of NDV-3 vaccine efficacy in MRSA skin versus invasive infection.Staphylococcus aureus alpha toxin suppresses effective innate and adaptive immune responses in a murine dermonecrosis model.Translational mini-review series on Th17 cells: function and regulation of human T helper 17 cells in health and disease.New mechanism of oral immunity to mucosal candidiasis in hyper-IgE syndrome.Transcriptional and epigenetic networks of helper T and innate lymphoid cells.Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis.IL-17A induces Pendrin expression and chloride-bicarbonate exchange in human bronchial epithelial cells Inflammation and repeated infections in CGD: two sides of a coin.Mitochondrial Ca²⁺ and membrane potential, an alternative pathway for Interleukin 6 to regulate CD4 cell effector function Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia.Regulation and function of innate and adaptive interleukin-17-producing cells Th17 cells, Job's syndrome and HIV: opportunities for bacterial and fungal infections Hyperimmunoglobulin E syndromes in pediatrics.

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Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome

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scientific article published on June 2009

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Molecular explanation for the ...... nfection in hyper-IgE syndrome

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Hidetoshi Takada

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Ikuya Tsuge

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Kazunaga Agematsu

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Masafumi Yamada

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Masako Saito

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Nobuaki Kawamura

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Shigeru Tsuchiya

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Tadashi Ariga

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Toshiro Hara

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Yoshiyuki Minegishi

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P2860

Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2

The biological functions of T helper 17 cell effector cytokines in inflammation

Cutting edge: interleukin 17 signals through a heteromeric receptor complex

STAT3 mutations in the hyper-IgE syndrome

Selective predisposition to bacterial infections in IRAK-4-deficient children: IRAK-4-dependent TLRs are otherwise redundant in protective immunity

TH17 cells in development: an updated view of their molecular identity and genetic programming

IL-22 increases the innate immunity of tissues

Interleukin-17 family members and inflammation

Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components

Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection

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1291-1301

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10.1084/JEM.20082767

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6

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206

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Hajime Karasuyama

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2009-06-01T00:00:00Z

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26258194

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19487419

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2715068

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