As indicated in Fig. Fig.5A5A both and and5B,5B, CD127 expression increased markedly in HBV-specific CD8 T cells in telbivudine responders compared with non-responders (P < 0.05). Figure 5 The emergence of CD127 hepatitis B virus (HBV)-specific CD8+ T cells after successful antiviral treatment. Surface staining of HBV-specific CD8 T cells was performed using a HBV multimer [A. HBV Core 18-27 (FLPSDFFPSV), B. HBV Core 18-27 (FLPSDFFPSI)] ... Discussion In our study, we demonstrated that CD127 expression on memory CD8 T cells was reduced in patients with CHB. There was a strong negative correlation between CD127 expression on memory CD8 T cells and serum HBV DNA and HBeAg levels in CHB patients. Moreover, successful antiviral therapy with telbivudine increased CD127 expression on CD8 memory T cells as well as on HBV-specific CD8 T cells in CHB patients.

It is widely accepted that CD8 T cells play an essential role in the immune response to viral infection. In successful responses to acute HBV, hepatitis C virus (HCV) and lymphocytic choriomeningitis virus (LCMV) infection, the up-regulation of CD127 expression on CD8 T cells is closely associated with the downregulation of CD38 and PD-1 and the upregulation of CCR7 expression [9,11,12]. All occurred in concert with resolution of disease and containment of viral antigen, supporting the theory that the emergence of CD127 is governed by withdrawal of antigenic stimulation. Colle et al. [13] reported that human immunodeficiency virus (HIV) infection was associated with a decrease in the proportion of CD127+ cells among memory CD8 T lymphocytes, which resulted in a higher CD127- CD8 T cells count in patients with HIV infection.

There was a strong negative correlation between CD127 expression on CD8 T cells and HIV viral load [14]. All of these results support the hypothesis that high CD127 expression on human CD8 T cells is specific for cleared virus [e.g. influenza virus, respiratory syncytial virus (RSV) and acute HBV infection] while low CD127 expression on human CD8 T cells is specific for persisting virus [e.g. HIV, cytomegalovirus (CMV), HCV and HBV] [15]. Recently some reports have suggested that CD127 might be a useful marker for predicting response Cilengitide to antiviral therapy in HIV- and HCV-infected patients. Badr et al. [11] reported that during HCV infection, early therapeutic intervention with pegylated (PEG)-interferon (IFN)-�� rescued long-lived, polyfunctional memory CD8 T cells expressing high levels of CD127 and Bcl-2 (CD127hiBclhi). In contrast, HCV-specific CD8 T cells in acute infections evolving to chronicity expressed low levels of CD127 and Bcl-2, exhibited diminished proliferation and cytokine production, and eventfully disappeared from the periphery. Colle et al.