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Chinese scientists reveal the mechanism of chronic hepatitis B infection leading to liver cancer

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Chinese scientists reveal the mechanism of chronic hepatitis B infection leading to liver cancer -Chinese-scientists-reveal-the-mechanism-of-chronic-hepatitis-B-infection-leading-to-liver-cancer

Academician Tian Zhigang of the University of Science and Technology of China revealed that chronic hepatitis B (HBV) infection can lead to the development of chronic hepatitis, cirrhosis and even liver cancer. The reporter learned from the University of Science and Technology of China that the TIGIT inhibitory pathway was maintained in transgenic mice by the Department of Life Sciences and Medicine, the Key Laboratory of Natural Immunology and Chronic Diseases of the Chinese Academy of Sciences, and the National Research Center of Hefei Microscale Material Science. The tolerance of CD8+ T cells to HBV, and breaking this tolerance can cause chronic inflammation of the liver in HBV transgenic mice (HBV carrying model), and eventually develop into liver cancer. On January 15th, the Nature Publishing Group's "Natural Communication" magazine published the research results online.

Chronic hepatitis B (HBV) infection can lead to chronic hepatitis, cirrhosis, and even liver cancer. Studies of chronic HBV infection have consistently lacked a suitable mouse model. The liver is a special immune-tolerant organ, and the immune cells in the liver are mainly immune-tolerant. In clinical HBV carriers and HBV transgenic mice, CD8+ T cells in the liver are immunosuppressed due to high expression of inhibitory receptors, and no liver damage occurs; and when the liver immune tolerance environment is broken, immune cells It is activated, and its immune response caused by the process of clearing the virus can cause liver inflammation.

The study found that HBV transgenic (HBs-tg) mice have high expression of the inhibitory receptor TIGIT, which can cause chronic hepatitis in mice by persistently blocking the TIGIT inhibitory pathway. The mice after TIGIT blockade are immunized with HBV surface antigen vaccine, and the mice can produce liver cancer. To explore the mechanism, the researchers found that the number of CD8+ T cells in the liver of HBs-tg mice increased after TIGIT blockade, activation increased, and antigen-specific CTLs appeared. HBs-tg mice that cleared CD8+ T cells significantly reduced liver damage after blocking TIGIT; if HBs-tg mice blocked by TIGIT cleared CD8+ T cells during vaccine immunization, they would not develop into liver cancer.

The study found that the TIGIT inhibitory pathway maintains the tolerance of CD8+ T cells in HBV-bearing mice, and successfully established a mouse model of liver cancer caused by chronic HBV infection, providing a follow-up study for the prevention and treatment of HBV-related liver cancer. A suitable animal platform.

(Original title Chronic hepatitis B infection leads to the mechanism of liver cancer)

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