ALLERGY, vol.75, no.4, pp.921-933, 2020 (Journal Indexed in SCI)
Article / Article
Title of Journal :
DOCK8, Hyper-IgE syndrome (HIES), ILC, ILC3, STAT3, INNATE LYMPHOID-CELLS, ROR-GAMMA-T, IMMUNE-DEFICIENCY, IL-7 RECEPTOR, DOCK8, MUTATIONS, DEDICATOR, EXPRESSION, IMMUNODEFICIENCY, GLYCOSYLATION
BackgroundDedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper-IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans.