Literature DB >> 22554706

TH17 deficiency in human disease.

Douglas R McDonald1.   

Abstract

The differentiation of naive T cells into distinct subsets of effector T cells is critical for effective immunity against a wide variety of infectious agents in the environment. Activation of innate immune responses by Candida species through pattern-recognition receptors directs the subsequent development of naive T cells into T(H)17 cells, which are essential for effective mucosal immunity against fungi. Thorough analyses of cohorts of patients with unusual susceptibility to chronic mucocutaneous candidiasis resulting from T(H)17 deficiency have confirmed the role of T(H)17 cells and T(H)17 cytokines in human host defense against Candida species and have provided valuable insights into the complex process of T(H)17 cell development.
Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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Year:  2012        PMID： 22554706      PMCID： PMC3388506          DOI： 10.1016/j.jaci.2012.03.034

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN： 0091-6749            Impact factor:   10.793


  48 in total

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Journal:  N Engl J Med       Date:  2011-06-29       Impact factor: 91.245

Review 8.  Signal transduction pathways and transcriptional regulation in Th17 cell differentiation.

Authors:  Kiyoshi Hirahara; Kamran Ghoreschi; Arian Laurence; Xiang-Ping Yang; Yuka Kanno; John J O'Shea
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3.  Candida albicans morphology and dendritic cell subsets determine T helper cell differentiation.

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5.  A STAT1-gain-of-function mutation causing Th17 deficiency with chronic mucocutaneous candidiasis, psoriasiform hyperkeratosis and dermatophytosis.

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Review 7.  The Ying and Yang of STAT3 in Human Disease.

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Review 8.  Primary immunodeficiency update: Part II. Syndromes associated with mucocutaneous candidiasis and noninfectious cutaneous manifestations.

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Review 10.  An Immunological Perspective on Neonatal Sepsis.

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