Abstract
Background: The imbalance of T-helper (Th) lymphocyte cytokine production plays an important role in the immunopathogenesis of chronic Hepatitis B Virus (HBV) infection. Th1 cytokines are necessary for host antiviral immune response, while Th2 cytokines have an immunomodulatory role. Objectives: The current study aimed at determining the serum profile of Th1 and Th2 cytokines in patients with chronic HBV infection and to assess the correlation between the levels of the cytokines and ALT level in the patients. Methods: Sixty patients with chronic hepatitis B and 60 age and gender-matched healthy controls were enrolled in the study. The serum levels of Th1 cytokine, interferon gamma (IFN-γ), Th2 cytokines, IL-4, and IL-10 were measured using the enzyme linked immunosorbent assay (ELISA). The serum ALT level was measured by the Colorimetry method. Results: The results showed that the level of IL-4 was significantly lower in patients in comparison with the controls (P 0.05). The concentration of IFN-γ was significantly higher in patients compared with the healthy controls (P < 0.05). No significant correlation was found between serum levels of IL-4, IL-10 and IFN-γ and nor was it found between the levels of these cytokines and serum ALT level. Conclusions: The results revealed enhanced Th1 response and reduced Th2 response, which is favored for the formation of a strong immune response and leads to viral elimination. The decrease of IL-4 indicated a lower viral load in the patients. In addition, a non-active disease resulted from the patients’ IL10 level showing no significant difference between the patients and the controls. Significant increase of IFN-γ in patients indicated the activation of Th1 cells. The immunological outcome can help in finding better treatment strategies. The results suggest that interferon therapy with low dose can be a helpful strategy. Although the decrease in ALT level was not significantly correlated with an increase in IFN-γ in the patients, the increase of IFN-γ level demonstrated a modulation in hepatocellular damage.
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