%0 Journal Article
%T Activated IL-23/IL-17 pathway closely correlates with increased Foxp3 expression in livers of chronic hepatitis B patients
%A Qinghong Wang
%A Yanhua Zheng
%A Zemin Huang
%A Yi Tian
%A Jijun Zhou
%A Qing Mao
%A Yuzhang Wu
%A Bing Ni
%J BMC Immunology
%D 2011
%I BioMed Central
%R 10.1186/1471-2172-12-25
%X Foxp3 expression was found to be elevated in and mainly expressed by the CD4+ T cell sub-population of peripheral blood mononuclear cells and liver tissues of patients with hepatitis B. The intrahepatic expression of Foxp3 strongly correlated with the copies of HBV DNA and the concentration of surface antigen, HBsAg. IL-23/IL-17 pathway-related proinflammatory cytokines were also found to be significantly increased in patients' liver tissues, as compared to healthy controls. Moreover, Foxp3 expression was strikingly correlated with the production of these cytokines in liver tissues of CHB patients.The closely-correlated increase of Foxp3 and IL-23/IL-17 pathway activity in HBV-infected livers suggests that the proinflammatory IL-23/IL-17 pathway had not been effectively suppressed by the host immune machinery, such as Treg (Foxp3) cells. Constitutive activation of the IL-23/17 pathway, thus, may support the chronic hepatitis B state.Hepatitis B virus (HBV) is a noncytopathic, hepatotropic DNA virus that is capable of inducing acute and chronic necroinflammatory liver injury [1]. Outcome of patients infected with HBV is closely associated with the extent of host immune response [2]. Moderate immune responses will mediate the clearance of HBV infection, while excessive responses will induce liver injury and low level responses will allow HBV residence. Unfortunately, patients with chronic hepatitis B (CHB) often exhibit impaired HBV-specific T cell responses [3]. The exact mechanisms of the immune system that fail in CHB infections remain unclear and, thus, remain a hindrance to the development of effective therapies.Many mechanisms have been hypothesized to explain the inadequate immune responses that facilitate chronic HBV infection. The most recent has focused on the dysfunction of regulatory T (Treg) cells. Treg cells are characterized by their cell-specific expression of Forkhead box P3 (Foxp3) [4], a transcription factor that contributes to autoimmune functions.
%K Treg
%K Foxp3
%K Th17
%K IL-23
%K IL-17
%K Hepatitis B
%U http://www.biomedcentral.com/1471-2172/12/25