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Viral Immunol. 2015 Aug 12. [Epub ahead of print]
Expression of PD-L1 on CD4+CD25+Foxp3+ Regulatory T Cells of Patients with Chronic HBV Infection and Its Correlation with Clinical Parameters.Feng C1, Cao LJ1, Song HF1,2,3, Xu P2,3, Chen H2,3, Xu JC2,3, Zhu XY2,3, Zhang XG1,4, Wang XF1.
Author information
- 11 Department of Biochemistry and Molecular Biology, School of Biology and Basic Medical Sciences, Soochow University , Suzhou, China .
- 22 Central Laboratory, The Affiliated Infectious Hospital of Soochow University , Suzhou, China .
- 33 Key Laboratory of Infection and Immunity of Suzhou City , Suzhou, China .
- 44 The First Affiliated Hospital of Soochow University , Suzhou, China .
AbstractRegulatory T cells (Tregs) play a pivotal role in suppressing specific antiviral immune responses during the progression of chronic hepatitis B virus infection (CHB) as well as tumorigenesis. Programmed death-1 ligand-1 (PD-L1) expressed on Tregs can transduce an inhibitory signal into effector T cells through interacting with programmed death-1 (PD-1). However, in CHB patients, the clinical significance of PD-L1 expression on Tregs has not been clearly described. This study investigated the frequency of circulating Tregs and PD-L1 expression on Tregs and analyzed their correlations with clinical parameters. The data show that both the frequency of CD4+CD25+FoxP3+ Tregs and PD-L1 expression on Tregs in the peripheral blood increased significantly in CHB patients when compared with healthy controls. At the same time, it is shown that PD-L1 expression on Tregs was positively correlated with the percentage of Tregs in CHB patients. Moreover, the results demonstrated that both Treg frequency and PD-L1 expression on Tregs positively correlated with the levels of alanine aminotransaminase (ALT) and aspartate aminotransferase (AST), both of which are indicators of the extent of liver injury. Taken together, these findings suggest that PD-L1 on Tregs might contribute to progression of hepatitis B virus infection through mediating the inhibitory function of Tregs. Thereby, blockade of interaction between Treg-expressing PD-L1 and PD-1 on effector T cells may be adopted as a potential therapeutic approach in CHB.
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