| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 102 === Hepatitis C virus (HCV) is a common cause of liver disease
worldwide. The persistent infection of HCV is associated with impaired
CD8 T cell function. Chronic infection can lead to fibrosis of the liver and
ultimately to cirrhosis, which is generally apparent after decades. In some
cases, those with cirrhosis will go on to develop liver cancer even die.
Human leukocyte antigen-DR (HLA-DR) and CD38 are expressed by
activated T cells during the acute phase of viral infections in humans.
Previous studied indicated that the populations of CD38+HLADR+CD8+ T
cells were increased when infected with Human Immunodeficiency Virus,
Epstein–Barr virus and Hepatitis B virus. However, the role of
CD38+HLADR+CD8+ T cells during chronic HCV infection is poor
described and their function has not been studied yet. In my study, results
showed that the percentage of CD38+HLADR+CD8+ T cells in peripheral
blood of chronic HCV patients was significantly increased when
compared with healthy volunteer. The CD38+HLADR+CD8+ T cells have
increased expression of cytotoxitc molecules but also with higher levels
of inhibitory receptor than CD38-HLADR-CD8+ T cells. In addition,
results showed these cells would accumulate in the inflamed liver. Results
indicated that the both HCV specific and non-HCV-specific CD8+ T cells
contributed to the increase of CD38+HLADR+CD8+ T cells in patients
with chronic hepatitis C. Moreover, the CD38+HLADR+CD8+ T cells
would behave as innate CD8+ T cells and produce IFN-γ by
cytokine-dependent pathway. Taken together, we suggest that during
chronic HCV infection, these CD38+HLADR+CD8+ T cells, both
HCV-specific and non-HCV specific, were increased and accumulated in
the liver. Their role in the chronic hepatitis C needs to be elicited in the
subsequent studies.
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