However, DOCK8-deficient B cells can present antigen to cognate CD4 T cells and are not rescued by BCR-independent delivery of antigen and T cell help via anti-DECOVA, suggesting that the primary B cell–intrinsic defect underlying the characteristic GC B cell loss in DOCK8 immunodeficiency is downstream of antigen gathering and presentation. This evidence concerns the gene DOCK8 and immunodeficiency disease.