Human immunodeficiency virus type 1 Tat induces B7-H1 expression via ERK/MAPK signaling pathway.

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.