Figure 2. Effect of HSCT on lymphocyte phenotype and differentiation in DOCK8-deficient patients.
PBMCs from healthy donors (n = 22–24), untransplanted DOCK8-deficient patients (n = 7–9), or DOCK8-deficient patients following HSCT (DOCK8 pHSCT) (n = 18–20) were labeled with mAbs against CD3, CD4, CD8, CD20, CD56, CD45RA, CCR7, CD10, CD27, IgM, IgD, TCRαβ, TCRγδ, TCRVα24, TCRVβ11, CD161, and TCR Vα7.2. Proportions of (A) CD3+ cells, CD4+ T cells (CD3+CD4+), CD8+ T cells (CD3+CD8+), B cells (CD20+); (B) CD8+ naive (CD45RA+CCR7+), central memory (TCM; CD45RA–CCR7+), effector memory (TEM; CD45RA–CCR7–), and CD45RA+ revertant memory (TEMRA; CD45RA+CCR7–) cells; (C) CD4+ naive, TCM, and TEM cell subsets; (D) αβ and γδ TCR+ T cells; (E) MAIT cells (CD3+TCRVα7.2+CD161+); (F) NK cells (CD3–CD56+); (G) NKT cells (CD3+TCRVα24+ Vβ11+); (H) transitional (Trans; CD20+CD10+CD27–), naive (CD20+CD10–CD27–), and memory (CD20+CD10–CD27+) B cell subsets; and (I) Ig class-switched memory (CD20+CD27+ IgD–IgM–) B cells were then determined by flow cytometric analysis. Contour plots represent 1 representative normal donor and 1 DOCK8-deficient patient before and after HSCT. Data are mean ± SEM. Statistical analysis was performed with GraphPad Prism using unpaired t test with Welch’s correction; *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001.