Article Type
Original Study
Abstract
Objective Our aim is to evaluate the expression of interleukin-17-producing CD4 + T cells (Th17) in peripheral blood of patients with chronic hepatitis B (CHB) and whether these cells show a potential to exacerbate liver damage during chronic hepatitis B virus (HBV) infection. Background Interleukin-17-producing CD4 + T cells (Th17)-mediated immune response has been shown to play a critical role in inflammation-associated disease; however, its role in chronic HBV infection remains unknown. Here, we characterized peripheral Th17 cells and analyzed their association with liver injury in HBV-infected patients. Participants and methods This study included 15 patients with CHB without cirrhosis (11 men and four women), 15 patients with CHB with cirrhosis (eight men and seven women), and 15 healthy controls (10 men and five women). Laboratory investigations including complete blood picture, liver function tests, hepatitis viral markers (HBsAg, anti-HCV-Ab), a-fetoprotein, and HBV DNA PCR were performed for all participants. Evaluation of the level of Th17 cells in the peripheral blood was carried out using the flow cytometry technique. Results The data showed that the frequency of circulating Th17 cells was increased in patients with CHB viral infection compared with the healthy controls, and was significantly higher in patients with CHB-associated cirrhosis. In addition, the increasing levels of circulating Th17 cells were correlated positively with serum alanine transaminase levels. Conclusion Our results showed that Th17 cells were highly enriched in the peripheral blood of CHB patients, and their levels were related to disease progression, suggesting its role in exacerbation of liver damage during chronic HBV infection.
Recommended Citation
El-Gazzar, Abeer A.; Zaghla, Hassan E.; El-Basuoni, Maha A.; Allam, Maha M.; and Soliman, Mohamed A.
(2014)
"Urinary 8-hydroxy-2'-deoxyguanosine as an oxidative DNA damage biomarker in chronic heart failure,"
Menoufia Medical Journal: Vol. 27:
Iss.
4, Article 27.
DOI: https://doi.org/10.4103/1110-2098.149753