Defects along the TH17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome
- 6 July 2009
- journal article
- research article
- Published by Elsevier in Journal of Allergy and Clinical Immunology
- Vol. 124 (2) , 342-348.e5
- https://doi.org/10.1016/j.jaci.2009.05.004
Abstract
No abstract availableKeywords
This publication has 36 references indexed in Scilit:
- Mutations in STAT3 and IL12RB1 impair the development of human IL-17–producing T cellsThe Journal of Experimental Medicine, 2008
- Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3 The Journal of Experimental Medicine, 2008
- Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndromeNature, 2008
- Transcriptional regulation of Th17 cell differentiationSeminars in Immunology, 2007
- Distinct regulation of interleukin‐17 in human T helper lymphocytesArthritis & Rheumatism, 2007
- Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17–producing human T helper cellsNature Immunology, 2007
- Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκBGenes & Development, 2007
- Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cellsNature, 2006
- Autosomal recessive hyperimmunoglobulin E syndrome: a distinct disease entityThe Journal of Pediatrics, 2004
- What does Stat3 do?Journal of Clinical Investigation, 2002