Abstract
No specific treatment can reverse the liver injury in cirrhosis. This study aims to characterize immune status and correlations between cirrhosis induced by HBV and HCV. Phenotypes of peripheral blood lymphocyte subsets (T, NK, regulatory T cells) and Th cytokine secretion were analyzed using flow cytometry in 42 HBV-cirrhotic and 40 HCV-cirrhotic patients. Cirrhotic patients had a lower proportion of CD3+CD8+T cells and NK cells, while the proportion of CD3+CD4+T cells and Treg cells were higher than those of healthy controls. The levels of Th2 cytokine (IL-6) in cirrhotic patients were increased, while only the Th1 cytokine (IFN-γ) increased in HBV-cirrhotic patients. These findings show that there is no difference between the cirrhotic groups except in the IFN-γ level. In cirrhosis, defects in innate, adaptive immune cells are likely regardless of which virus is involved. A cytokine imbalance may play a role in the development of posthepatitic cirrhosis.
Highlights
Cirrhosis is the twelfth leading cause of death, accounting for 27,000 deaths each year worldwide
There were no significant differences in lymphocyte subsets between the two cirrhotic groups
The CD4/CD8 ratio and CD3+CD4+ cells were higher, while the CD3+CD8+Foxp3+ cells and NK cells were lower in the cirrhosis groups than in the healthy control group
Summary
Cirrhosis is the twelfth leading cause of death, accounting for 27,000 deaths each year worldwide. It is caused mostly by hepatitis B and C infection, alcoholism, and autoimmune liver diseases. Hepatitis B virus is probably the most common cause of cirrhosis in most of the world, but in the United States and Western countries, chronic alcoholism and hepatitis C are the most common causes [1]. Conventional treatment for cirrhosis can stop or slow progression of the disease and reduce complications, but it cannot reverse liver damage. Understanding the disease process, making appropriate risk stratification, and implementing treatment require a valid and precise understanding of the immune status
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