CD38
脱颗粒
CD16
免疫学
CD8型
推车
先天免疫系统
免疫系统
流式细胞术
新喋呤
锡克
CD19
医学
生物
内科学
CD3型
酪氨酸激酶
受体
川地34
细胞生物学
工程类
机械工程
干细胞
作者
Gregor F. Lichtfuss,Wan-Jung Cheng,Yagmur Farsakoglu,Geza Paukovics,Reena Rajasuriar,Pusparaj Velayudham,Marit Kramski,Anna C. Hearps,Paul Cameron,Sharon R. Lewin,Suzanne Crowe,Anthony Jaworowski
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2012-08-01
卷期号:189 (3): 1491-1499
被引量:105
标识
DOI:10.4049/jimmunol.1200458
摘要
Abstract FcRγ is an ITAM-containing adaptor required for CD16 signaling and function in NK cells. We have previously shown that NK cells from HIV patients receiving combination antiretroviral therapy (cART) have decreased FcRγ expression, but the factors causing this are unknown. We conducted a cross-sectional study of cART-naive viremic patients (ART−), virologically suppressed patients receiving cART (ART+), and HIV-uninfected controls. CD8+ T cells were activated, as assessed by CD38+HLA-DR+ expression, in ART− patients (p < 0.0001), which was significantly reduced in ART+ patients (p = 0.0005). In contrast, CD38+HLA-DR+ NK cells were elevated in ART− patients (p = 0.0001) but did not decrease in ART+ patients (p = 0.88). NK cells from both ART− and ART+ patients showed high levels of spontaneous degranulation in ex vivo whole blood assays as well as decreased CD16 expression (p = 0.0001 and p = 0.0025, respectively), FcRγ mRNA (p < 0.0001 for both groups), FcRγ protein expression (p = 0.0016 and p < 0.0001, respectively), and CD16-dependent Syk phosphorylation (p = 0.0001 and p = 0.003, respectively). HIV-infected subjects showed alterations in NK activation, degranulation, CD16 expression and signaling, and elevated plasma markers of inflammation and macrophage activation, that is, neopterin and sCD14, which remained elevated in ART+ patients. Alterations in NK cell measures did not correlate with viral load or CD4 counts. These data show that in HIV patients who achieve viral suppression following cART, NK cell activation persists. This suggests that NK cells respond to factors different from those driving T cell activation, but which are associated with inflammation in HIV patients.
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