Foxp3+Helios+ regulatory T cells are associated with monocyte subsets and their PD-1 expression during acute HIV-1 infection
Foxp3+Helios+ regulatory T cells are associated with monocyte subsets and their PD-1 expression during acute HIV-1 infection
复制标题
Foxp3( )Helios( ) 调节性 T 细胞与急性 HIV-1 感染期间的单核细胞亚群及其 PD-1 表达相关
DOI:
10.1186/s12865-019-0319-7
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发表时间:
2019-10-24
期刊:
影响因子:
3
通讯作者:
Zhang, Tong
中科院分区:
文献类型:
--
作者:
Liu, Lifeng;Zhang, Qiuyue;Zhang, Tong
Background Helios has been reported to stabilize regulatory T (Treg) suppressive function. Programmed cell death protein 1 (PD-1) expression in three human monocyte subsets modulates immune responses. Recently, our team reported that three monocyte subsets are associated with T helper cell differentiation in HIV-1-infected patients. Until now, the effects of monocyte subsets and their PD-1 expression on Foxp3(+)Helios(+) Treg cells have not been fully characterized, especially during acute HIV-1 infection. Results The frequency of Foxp3(+)Helios(+)CD45RA(+) Treg cells is significantly higher in patients with acute HIV-1 infection than those of healthy controls and chronic HIV-1-infected patients undergoing combined antiretroviral therapy. The frequency of Foxp3(+)Helios(+)CD45RA(+) Treg cells is inversely correlated with CD4 T-cell counts and the CD4/CD8 ratio in chronic HIV-1-infected patients. During acute HIV-1 infection, the frequency of Foxp3(+)Helios(+)CD45RA(+) Treg cells is inversely correlated with the frequency of the intermediate CD14(++)CD16(+) monocyte subset, but positively correlated with PD-1 expression in both intermediate CD14(++)CD16(+) and non-classical CD14(+)CD16(++) monocyte subsets. Conclusions In this study, the perturbations of Foxp3(+)Helios(+) Treg cells were characterized, and the association between monocyte subsets and their PD-1 expression and Foxp3(+)Helios(+) Treg cells was evaluated during HIV-1 infection. Our observations provide new evidence of the roles for Foxp3(+)Helios(+) Treg cells and PD-1 expression on monocyte subsets in HIV pathogenesis.