Published January 1, 2016
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Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T(H)17 cell differentiation
Creators
- 1. Boston Childrens Hosp, Harvard Med Sch, Div Immunol, Boston, MA USA
- 2. Boston Childrens Hosp, Harvard Med Sch, Dept Pediat, Program Mol & Cellular Med, Boston, MA USA
- 3. Necmettin Erbakan Univ, Meram Med Fac, Div Pediat Immunol & Allergy, Konya, Turkey
- 4. Behcet Uz State Hosp, Div Pediat Immunol, Izmir, Turkey
- 5. Kuwait Univ, Fac Med, Dept Pediat, Kuwait, Kuwait
- 6. Boston Childrens Hosp, Harvard Med Sch, Dept Pathol, Boston, MA USA
Description
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 T(H)17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear.
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