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ABSTRACT: Background
The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokinesis 8 (DOCK8) deficiency shares clinical features with autosomal dominant HIES because of signal transducer and activator of transcription 3 (STAT3) mutations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear.Objective
We sought to elucidate common mechanisms operating in the different forms of HIES.Methods
We analyzed the differentiation of CD4+ TH cell subsets in control and DOCK8-deficient subjects. We also examined the role of DOCK8 in regulating STAT3 activation in T cells. TH cell differentiation was analyz
SUBMITTER: Keles S
PROVIDER: S-EPMC5099100 | biostudies-literature | 2016 Nov
REPOSITORIES: biostudies-literature