期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 36, 期 2, 页码 278-286出版社
WILEY
DOI: 10.1002/eji.200535487
关键词
CD1; HIV; innate immunity; Nef
类别
资金
- Medical Research Council [G0400720, MC_U137881015] Funding Source: researchfish
- MRC [MC_U137881015, G0400720] Funding Source: UKRI
- Medical Research Council [G0400720, MC_U137881015] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
HIV-1 has evolved several strategies to subvert host immune responses to the infected cells. One is to inhibit CTL recognition by HIV-1 Nef-mediated down-regulation of MHC-I expression on the surface of infected cells. Here we report that Nef also reduces the expression of the non-classical MHC-I like CD1d molecule, a third lineage of antigen-presenting molecule, which presents lipid antigens. Nef achieves this by increasing internalization of CD1d molecules from the cell surface and retaining CD1d in the trans-Golgi-network (TGN). This effect depends on a tyrosine-based motif present in CD1 cytoplasmic tail as well as the actions of four Nef motifs, which are known to be involved in the down-regulation of MHC-I or CD4. These results suggest that Nef regulates intracellular trafficking of CD1d via a distinct but shared pathway with MHC-I and CD4. Thus, HIV-1 reduces the visibility of its infected cells not only to MHC-I-restricted T cells but also to CD1d-restricted NKT cells. Given that CD1d-restricted T cells have unique effector and regulatory functions in innate and adapted immune responses as compared with their counterpart MHC-restricted T cells, our data provide additional new insights into molecular basis of HIV-1-mediated damage to the immune system.
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