کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2167281 | 1092323 | 2011 | 6 صفحه PDF | دانلود رایگان |
In HIV-infected subjects, B7-H1 synthesis and expression are up-regulated, and the degree of dysregulation correlates with the severity of disease. HIV-1 Tat protein, the viral transactivating factor, represents a key target for the host immune response. However, the relationship between B7-H1 and Tat protein has not been addressed. Here, we chose human endothelial cells which provide costimulatory signals sufficiently to influence T cells. We used recombinant pcDNA3.1(+)–Tat plasmid to transfect human endothelial cells ECV304 to establish stable Tat-expressed cell strain, and found that HIV-1 Tat was able to induce B7-H1 expression in ECV304 cells by Real-time PCR and flow cytometry analysis, and inhibited lymphocyte proliferation in co-culture system. Moreover, by using pharmacological inhibitor of ERK pathway, HIV-1 Tat induces B7-H1 expression via ERK/MAPK signaling pathway was corroborated. In summary, our results indicate that HIV-1 Tat could induce B7-H1 synthesis in ECV304 cells through ERK/MAPK signaling pathway.
► B7-H1 was up-regulated and correlated with the severity of disease in AIDS patients.
► HIV-1 Tat plays a key role in the viral replication and host immune regulation.
► We established stable Tat-expressed cell strain in human endothelial cells ECV304.
► HIV-1 Tat induced B7-H1 over-expression and inhibited lymphocyte proliferation.
► HIV-1 Tat up-regulated B7-H1 expression via ERK/MAPK signaling pathway.
Journal: Cellular Immunology - Volume 271, Issue 2, 2011, Pages 280–285