Renal tubular epithelial expression of the coinhibitory molecule B7-DC (programmed death-1 ligand).
BACKGROUND: Renal tubular epithelial cells (TECs) function as antigen-presenting cells because they constitutively express MHC class II molecules and have the ability to present peptide antigen to CD4+T cells. However, the costimulatory signals provided by TECs for optimal T-cell activation have not been fully characterized. Increasing recognition of the importance of B7 dendritic cells (B7-DC) in immunoregulation raises the question of whether B7-DC is expressed on TECs and is involved in regulating TEC function. METHODS: B7-DC on cultured human and murine TECs was detected by flow cytometry in vitro. Immunohistochemistry was performed on human kidney biopsies. Coculture experiments were performed to confirm the role of TEC-related B7-DC in regulating CD4+T-cell activation. RESULTS: Data revealed that B7-DC is specifically expressed on TECs with inflammatory factor induced and diseased human kidney samples, including chronic glomerulonephritis, lupus nephritis, tubulointerstitial nephritis and renal cell carcinoma. B7-DC was a strong inhibitor of CD4+T-cell activation, as assessed by increased cytokine (interferon-gamma and interleukin-2) production and enhanced levels of T-cell activation marker CD69 in the presence of its blocking antibody. Blocking B7-DC/PD-1 enhanced antigen presentation. B7-DC is especially well expressed on TECs of diseased kidney samples and significantly down-regulates T-cell activation. CONCLUSIONS:We speculate that B7-DC might play an important role in maintaining peripheral tolerance, and in protecting the epithelium from immune-mediated tubulointerstitial injury.[1]References
- Renal tubular epithelial expression of the coinhibitory molecule B7-DC (programmed death-1 ligand). Zhang, J., Chen, Y., Li, J., Zhang, R., Wu, Y., Zou, L., Zhao, T., Zhang, X., Han, J., Chen, A., Wu, Y. J. Nephrol. (2006) [Pubmed]
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