Defects along the TH17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome

17 publications in the local catalog that cite this work (OpenAlex reference match; not the full global list).

1. 2009 Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndromeCitations 534 · OpenAlex
2. 2009 Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndromeCitations 530 · OpenAlex
3. 2009 Large deletions and point mutations involving the dedicator of cytokinesis 8 DOCK8 in the autosomal recessive form of hyper IgE syndromeCitations 530 · OpenAlex
4. 2009 Large deletions and point mutations involving the dedicator of cytokinesis 8 DOCK8 in the autosomal recessive form of hyper IgE syndromeCitations 530 · OpenAlex
5. 2018 ZNF341 controls STAT3 expression and thereby immunocompetenceCitations 154 · OpenAlex
6. 2014 Dedicator of cytokinesis 8–deficient patients have a breakdown in peripheral B-cell tolerance and defective regulatory T cellsCitations 100 · OpenAlex
7. 2016 Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes TH17 cell differentiationCitations 97 · OpenAlex
8. 2016 Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes TH17 cell differentiationCitations 97 · OpenAlex
9. 2023 Severe Allergic Dysregulation due to a Gain of Function Mutation in the Transcription Factor STAT6Citations 69 · OpenAlex
10. 2023 Severe allergic dysregulation due to a gain of function mutation in the transcription factor STAT6Citations 69 · OpenAlex