期刊
WORLD ALLERGY ORGANIZATION JOURNAL
卷 5, 期 -, 页码 79-87出版社
BIOMED CENTRAL LTD
DOI: 10.1097/WOX.0b013e31825a73b2
关键词
STAT3; DOCK8; TYK2; T(H)17; Job syndrome; Hyper-IgE syndrome; immunodeficiency
Hyper-IgE syndrome is a primary immunodeficiency marked by abnormalities in the coordination of cell-cell signaling with the potential to affect T(H)17 cell, B cell, and neutrophil responses. Clinical manifestations include recurrent skin and lung infections, serum IgE elevation, connective tissue repair and development alterations, and the propensity for vascular abnormalities and tumor development. Signal transducer and activator of transcription 3 (STAT3) signaling, dedicator of cytokinesis 8 (DOCK8) signaling, and tyrosine kinase 2 (TYK2) signaling alterations have been implicated in 3 forms of hyper-IgE syndrome.
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