Ascertain the effects of disease-causing gene mutations on the differentiation status of human nave CD4+ T cells in the setting of primary immunodeficiencies. Thus, do CD4+ T cells isolated according to a nave surface phenotype (ie CD4+CD45RA+CCR7+) from healthy donors exhibit a similar gene expression profile as phenotpyically-matched cells isolated from individuals with defined primary immunodeficiencies caused by specific monogenic mutations.
Unique and shared signaling pathways cooperate to regulate the differentiation of human CD4+ T cells into distinct effector subsets.
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