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. 2017 Jul 17;8:798. doi: 10.3389/fimmu.2017.00798

Figure 7.

Figure 7

(A) Percentage of NKG2C+ cells among CD3 CD19 CD14 CD56+ cells from patients and controls. (B) Percentage of NKG2C+ cells among natural killer (NK) cells from patients with recombinase-activating gene (RAG)/non-homologous end-joining (NHEJ) defects with positive (+) or negative (−) history of infections due to cytomegalovirus (CMV), Epstein–Barr virus (EBV), varicella zoster virus (VZV), or JC virus (JCV). (C) Percentage of NKG2C+ cells among NK cells from patients with RAG/NHEJ defects presenting with severe combined immune deficiency (SCID), Omenn syndrome/atypical SCID (SCID/OS/AS), or with delayed onset combined immune deficiency (CID), and divided into two groups according to the presence (+) or absence (−) of a history of CMV infection. (D) Percentage of CD56dim CD16+ cells among NK cells from patients with RAG/NHEJ defects presenting with SCID/OS/AS or with CID, and with either positive (+) or negative (−) history of CMV infection. (E) Percentage of CD56 CD16+ CD57+ cells among CD3 CD14 CD20 peripheral blood mononuclear cells. Bars represent mean ± SD values. *p < 0.05; **p < 0.01; ***p < 0.005.