Dock8 mutation impairs the differentiation of helper T cells by regulating the glycolytic pathway of CD4+ T cells

Dedicator of cytokinesis 8 (DOCK8) deficiency is a primary immunodeficiency disease caused by mutations in exon 45 of the Dock8 gene. Its Clinical manifestations mainly include elevated serum IgE levels, eczema, recurrent skin infections, allergies, and upper respiratory tract infections. We employed CRISPR/Cas9 technology to construct a Dock8 exon 45 mutation in mice that is equivalent to that in patients. Our research elucidates that DOCK8 regulates the differentiation of helper T cells by modulating the glycolytic pathway in CD4+ T cells, contributing to a better understanding and potential treatment of diseases in patients with DOCK8 deficiencies.