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Background
Inherited chronic mucocutaneous candidiasis (CMC) is often caused by inborn errors of immunity, impairing the response to, or the production of IL‐17A and IL‐17F. About half of the cases carry STAT1 gain‐of‐function (GOF) mutations. Only few patients have been reported with mutations of TRAF3IP2, a gene encoding the adaptor ACT1 essential for IL‐17 receptor(R) signaling. We investigated...
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