الفهرس | Only 14 pages are availabe for public view |
Abstract TLRs are involved in innate immunity. Certain viruses- including HCV- interact with TLRs and mediate antiviral effects as well as immune responses. With recent research progress, the possibility of cytokine regulation and the modulation of TLR function for therapeutic purposes became realistic. It is essential to study the mechanisms of HCV activation of immune cells and indicate a new, potential direction in managing the imbalanced immune functions during chronic infection with HCV. The aim of this study was to determine the expression of TLR2 on peripheral blood monocytes of patients with liver cirrhosis complicating chronic hepatitis C infection as compared to normal individuals, to measure serum levels of TNF- α, and to correlate between TLR2 expression and serum TNF- α level in those patients. This may help to investigate the effect of TLR-2 expression on modification of TNF- α as a vital part in the pathogenesis in HCV-infected patients complicated with liver cirrhosis. This study included two groups. Group I comprised 40 patients with liver cirrhosis complicating chronic HCV infection, selected from Department of Tropical medicine, Ain Shams University Hospital. Group II included 20 apparently healthy individuals with no past history of liver disease and negative for HCV antibodies. Venous blood samples were collected from each subject for assessment of TLR2 expression on peripheral blood monocytes via flowcytometric analysis and measurement of TNF-α serum levels via EIA. Increased TLR2 expression in peripheral blood monocytes was detected among patients and positive correlation was detected between the increased serum TNF- α levels and increased TLR2 expression among patients. In conclusion, there is an evidence that the up regulation of TLR2 expression in peripheral blood monocytes contributes to the increase of circulating TNF-α in patients with liver cirrhosis complicating HCV infection, suggesting the possible targeting of TLR-2 as a tool to decrease TNF-α levels in those patients in the future with subsequent limitation of the progression of liver cirrhosis with its devastating complications. |