Abstract
BackgroundFoxp3 protein plays a critical role in mediating the inflammatory response and can inhibit the proinflammatory IL-23/IL-17 pathway. However, the molecular interplay of Foxp3 and the IL-23/IL-17 pathway in patients with chronic hepatitis B (CHB) remains unclear. To this end, we analyzed the expression patterns of Foxp3- and IL-23/IL-17 pathway-related proinflammatory cytokines in 39 patients with acute-on-chronic liver failure, 71 patients with CHB and 32 healthy controls.ResultsFoxp3 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.ConclusionsThe 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.
Highlights
Forkhead box P3 (Foxp3) protein plays a critical role in mediating the inflammatory response and can inhibit the proinflammatory IL-23/IL-17 pathway
Foxp3 expression is significantly high in peripheral blood of chronic hepatitis B (CHB) patients Tregs with transcription factor Foxp3 play an pivotal role in controlling immune response mediated inflammation [16]
Foxp3 is significantly augmented in liver tissue of patients infected with Hepatitis B virus (HBV) To further value the role of Foxp3 in patients with hepatitis B, we detected the expression level of Foxp3 in liver tissue from patients infected by HBV by using qPCR and immunohistochemistry techniques
Summary
Foxp protein plays a critical role in mediating the inflammatory response and can inhibit the proinflammatory IL-23/IL-17 pathway. The molecular interplay of Foxp and the IL-23/IL-17 pathway in patients with chronic hepatitis B (CHB) remains unclear. To this end, we analyzed the expression patterns of Foxp3and IL-23/IL-17 pathway-related proinflammatory cytokines in 39 patients with acute-on-chronic liver failure, 71 patients with CHB and 32 healthy controls. The intrahepatic expression of Foxp strongly correlated with the copies of HBV DNA and the concentration of surface antigen, HBsAg. IL-23/IL-17 pathway-related proinflammatory cytokines were found to be significantly increased in patients’ liver tissues, as compared to healthy controls. Patients with chronic hepatitis B (CHB) often exhibit impaired HBV-specific T cell responses [3]. In HBV patients, Foxp3+ Treg cells have been associated with the incidence and extent of liver damage [6,7,8,9,10]
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