Defects along the T(H)17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome. - Wikidata - wikimedia - TriplyDB

Defects along the T(H)17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome.

Defects along the T(H)17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome.

http://www.wikidata.org/entity/Q33686966

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The hyperimmunoglobulin E syndrome--clinical manifestation diversity in primary immune deficiency Actin cytoskeletal defects in immunodeficiency Mendelian genetics of human susceptibility to fungal infection The Hyper-IgE Syndromes: Lessons in Nature, From Bench to Bedside STATs in cancer inflammation and immunity: a leading role for STAT3 Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndrome.Advances in basic and clinical immunology in 2009 Cellular and Molecular Defects Underlying Invasive Fungal Infections-Revelations from Endemic Mycoses.Cutaneous manifestations of DOCK8 deficiency syndrome Dedicator of cytokinesis 8 (DOCK8) deficiency Successful engraftment of donor marrow after allogeneic hematopoietic cell transplantation in autosomal-recessive hyper-IgE syndrome caused by dedicator of cytokinesis 8 deficiency.Deficient T Cell Receptor Excision Circles (TRECs) in autosomal recessive hyper IgE syndrome caused by DOCK8 mutation: implications for pathogenesis and potential detection by newborn screening.Dedicator of cytokinesis 8-deficient patients have a breakdown in peripheral B-cell tolerance and defective regulatory T cells.Educational paper: syndromic forms of primary immunodeficiency Th17 cells, Job's syndrome and HIV: opportunities for bacterial and fungal infections Hyperimmunoglobulin E syndromes in pediatrics.The Ying and Yang of STAT3 in Human Disease Genetic Susceptibility to Fungal Infections in Humans.Warts and all: human papillomavirus in primary immunodeficiencies.Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis.Chronic mucocutaneous candidiasis: characterization of a family with STAT-1 gain-of-function and development of an ex-vivo assay for Th17 deficiency of diagnostic utility.T cell transcriptional factors in allergic rhinitis and its association with clinical features.Effects of Photodynamic Therapy Using Yellow LED-light with Concomitant Hypocrellin B on Apoptotic Signaling in Keloid Fibroblasts.Diffuse large B cell lymphoma in hyper-IgE syndrome due to STAT3 mutation.Pediatric allergy and immunology in Turkey.Immunity against Staphylococcus aureus cutaneous infections.Innate and adaptive immune responses against Staphylococcus aureus skin infections.DOCK8 deficiency.TH17 deficiency in human disease.Emerging new roles of Th17 cells.Skin manifestations of primary immune deficiency.ICON: the early diagnosis of congenital immunodeficiencies.Primary Immunodeficiencies with Elevated IgE.Patterns of Primary Immunodeficiency Disorders Among a Highly Consanguineous Population: Cairo University Pediatric Hospital's 5-Year Experience.Genetic Predictors of Susceptibility to Dermatophytoses.Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes TH17 cell differentiation.Key findings to expedite the diagnosis of hyper-IgE syndromes in infants and young children.A novel large deletion of the DOCK8 gene in a Chinese family with autosomal-recessive hyper-IgE syndrome.Inhibition of STAT3 Signaling Reduces IgA1 Autoantigen Production in IgA Nephropathy.DOCK8: regulator of Treg in response to corticotropin-releasing hormone.

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P2860

Defects along the T(H)17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome.

http://www.wikidata.org/entity/Q33686966

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2009 nî lūn-bûn

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2009年の論文

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Defects along the T(H)17 diffe ...... rms of the hyper IgE syndrome.

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Ali Baki

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Anupama Rambhatla

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Aydan Ikinciogullari

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Ayper Somer

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Derek W Nickerson

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Elif Karakoc-Aydiner

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Ercan Kucukosmanoglu

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Ferah Genel

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Haluk Cokugras

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Hasibe Artac

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P2860

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

Hyper-IgE syndrome with recurrent infections--an autosomal dominant multisystem disorder

Job's Syndrome. Recurrent, "cold", staphylococcal abscesses

STAT3 mutations in the hyper-IgE syndrome

Extreme hyperimmunoglobulinemia E and undue susceptibility to infection

Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity

Structure, function, and regulation of STAT proteins

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

IL-6 programs T(H)-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways

Essential autocrine regulation by IL-21 in the generation of inflammatory T cells

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