HIV-1衍生的Toll样受体配体对单核细胞和树突状细胞上PD-L1的上调作用。
Upregulation of PD-L1 on monocytes and dendritic cells by HIV-1 derived TLR ligands.
作者信息
Meier Angela, Bagchi Aranya, Sidhu Harlyn K, Alter Galit, Suscovich Todd J, Kavanagh Daniel G, Streeck Hendrik, Brockman Mark A, LeGall Sylvie, Hellman Judith, Altfeld Marcus
机构信息
Partners AIDS Research Center, Massachusetts General Hospital, Division of AIDS, Harvard Medical School, Boston, Massachusetts, USA.
出版信息
AIDS. 2008 Mar 12;22(5):655-8. doi: 10.1097/QAD.0b013e3282f4de23.
Abstract
Increased PD-L1 expression has been reported in HIV-1-infected individuals, but the mechanisms leading to PD-L1 upregulation remain to be elucidated. Here we demonstrate that HIV-1-derived Toll-like receptor (TLR)7/8 ligands can induce MyD88-dependent upregulation of PD-L1 on plasmacytoid dendritic cells, myeloidic dendritic cells and monocytes. These data suggest a mechanism through which HIV-1-derived TLR ligands might contribute to the functional impairment of virus-specific PD-1-positive T cells by inducing the upregulation of PD-L1 on antigen-presenting cells.
摘要
据报道，HIV-1感染个体中PD-L1表达增加，但导致PD-L1上调的机制仍有待阐明。在此，我们证明HIV-1衍生的Toll样受体（TLR）7/8配体可诱导浆细胞样树突状细胞、髓样树突状细胞和单核细胞上MyD88依赖的PD-L1上调。这些数据提示了一种机制，通过该机制HIV-1衍生的TLR配体可能通过诱导抗原呈递细胞上PD-L1的上调，导致病毒特异性PD-1阳性T细胞功能受损。
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