Blocking gene boosts T-cell attacks on chronic hepatitis B virus and tumors

A research team led by Professor Zhou Xuyu from the Institute of Microbiology of the Chinese Academy of Sciences (CAS), in collaboration with researchers from Beijing Ditan Hospital and Capital Medical University, has identified ANKRD11 as a key regulator that reduces the activity of CD8+ T cells during chronic hepatitis B virus (HBV) infection and cancer. The researchers found that ANKRD11 suppresses the AP-1 signaling pathway, which usually helps CD8+ T cells mount effective responses against infections and tumors.

HBV infects about 296 million people worldwide and is a leading cause of serious liver diseases such as cirrhosis and liver cancer. One major reason the immune system struggles to control chronic HBV is that CD8+ T cells, which normally attack infected cells, become weakened and can’t multiply well. The liver environment can further suppress immune responses, making some existing immune-based therapies less effective against HBV. Identifying new ways to restore T cell function is therefore an important goal in treating chronic HBV infection.

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