Expression Profiles of Circulating Cytokines, Chemokines, and Immune Cells in Patients With Hepatitis B Virus Infection

Loading...
Thumbnail Image

Journal Title

Journal ISSN

Volume Title

Publisher

Brieflands

Abstract

Background: Immune cells and molecules play a vital role in initiating, maintaining, and regulating immunological homeostasis and inflammation in many pathological and physiological processes; however, the changes on expressions and functions of these cells and molecules in hepatitis B virus (HBV) infection has not been elucidated well. Objectives: The current study aimed to determine the expression pattern of different cytokines, chemokines, and immune cells in HBV infection and their association with disease progression. Materials and Methods: Sixty-nine patients with chronic HBV infection were enrolled. Five immune cell subsets and 46 cytokines and chemokines were analyzed by flow cytometry and Luminex 200. Results: In comparison to healthy individuals and asymptomatic HBV carriers, expression of CXCL9, CXCL10, CXCL11, and IL-10 were elevated in patients with chronic active HBV and had positive correlation with ALT levels. In contrast, G-CSF, MCP-3, and IFN-γ levels were significantly decreased in patients with chronic active HBV infection in contrast to carriers and healthy individuals; however, these down regulations did not show any correlation with either virological findings or liver inflammation. Although the proportion of CD4+ CD25high regulatory T cells (Tregs) was higher in patients with HBV infection than in healthy controls, no correlations were found between Tregs and other cytokines or chemokines. Conclusions: CXCR3-associated chemokines might contribute to liver inflammation in chronic hepatitis B, while MCP-3 and G-CSF were inhibited by HBV infection. Host immune response was suppressed as manifested by an increase in CD4+ CD25high Tregs and IL-10 as well as a decrease in IFN-γ. Exploiting the expression pattern of cytokine and chemokine may help to develop a better understanding of chronic HBV infection pathogenesis.

Description

Keywords

Citation

URI

Endorsement

Review

Supplemented By

Referenced By