Eken A, Cansever M, Okus FZ, et al. - Given autosomal recessive hyper IgE syndrome (HIES) is mainly caused by the deficiency of dedicator of cytokinesis 8 (DOCK8), and a Dock8-deficient mouse model exhibited the selective loss of group 3 innate lymphoid cell (ILC) number and function in a previous report, therefore, researchers investigated if DOCK8 is needed for the function and maintenance of ILC subsets in humans. Using flow cytometry and real time qPCR, they compared peripheral blood ILC1-3 subsets of 16 DOCK8-deficient patients selected at the pretransplant stage, and seven patients with autosomal dominant HIES because of STAT3 mutations vs those of healthy controls or posttransplant DOCK8-deficient patients (n = 12). Findings revealed DOCK8 as a regulator of human ILC3 expansion and survival. More globally, it regulated ILC cytokine signaling and proliferation. Loss of ILC3 from peripheral blood was caused by DOCK8 deficiency. A possible contribution of ILC3 deficiency to susceptibility to infections in DOCK8-deficient patients was suggested.