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. 2019 Jun 6;4(11):e127527. doi: 10.1172/jci.insight.127527

Figure 4. HSCT overcomes CD8+ T cell functional defects due to DOCK8 deficiency.

Figure 4

CD8+ T cells were sorted from the peripheral blood of healthy donors (n = 18–26), untransplanted DOCK8-deficient patients (n = 2–7), and DOCK8-deficient patients following HSCT (DOCK8 pHSCT) (n = 13–18); labeled with CFSE; and then cultured with TAE (anti-CD2/CD3/CD28) beads in the absence or presence of IL-2. After 5 days, culture supernatants were collected, and cells were harvested and then restimulated with PMA/ionomycin for 6 hours, with brefeldin A, monensin, and anti-CD107a mAb being added after 1 hour. (A) The frequency of cells in each division was determined by dilution of CFSE. (B) Expression of CD107a and (C) secretion of granzyme A and granzyme B were determined by flow cytometry and cytometric bead arrays, respectively. (D) Surface expression of CD25 and (E) CD95 was determined by flow cytometry. (F and G) Secretion of IFN-γ, TNF-α, and IL-2 was determined by cytometric bead arrays. Histograms in A, B, D, and E are representative of one healthy donor and one paired DOCK8-defcient patient before and after HSCT. Data represent the mean ± SEM. Statistics performed using Prism unpaired t test with Welch’s correction *P < 0.05, **P < 0.01, ***P < 0.005.