国际肝脏病学著名期刊《肝脏学》（Hepatology）于2009年9月发表了CD24分子影响慢性乙肝病毒感染以及疾病进程的最新研究成果，这一工作由中科院生物物理研究所王盛典课题组、美国密歇根大学刘阳教授、以及中国人民解放军302医院的王福生教授合作共同完成，其论文题为CD24 polymorphisms affect risk and progression of chronic hepatitis B virus infection。
CD24 polymorphisms affect risk and progression of chronic hepatitis B virus infection
Dongling Li 1, Linghua Zheng 1 2, Lei Jin 3, Yuesu Zhou 3, Haiying Li 4, Junliang Fu 3, Ming Shi 3, Peishuang Du 1, Lizhong Wang 5, Hao Wu 4, Guo-Yun Chen 5, Pan Zheng 5 6, Yang Liu 1 5 *§, Fu-Sheng Wang 1 3 *, Shengdian Wang 1 *
1Center for Infection and Immunity, National Laboratory of Biomacromolecules, Institute of Biophysics, Beijing, China
2Graduate School of Chinese Academy of Sciences, China Chinese Academy of Sciences, Beijing, China
3Research Center for Biological Therapy, Beijing 302 Hospital, Beijing, China
4Beijing You-An Hospital, Capital Medical University, Beijing, China
5Division of Immunotherapy, University of Michigan, Ann Arbor, MI
6Department of Surgery, Comprehensive Cancer Center and Program of Molecular Mechanisms of Disease, University of Michigan, Ann Arbor, MI
T-cell immunity to hepatitis B virus (HBV) is involved in both viral clearance and the pathogenesis of cirrhosis and hepatocellular carcinoma following chronic HBV infection. It is therefore of great interest to analyze whether genetic polymorphism of genes involved in the immune response may determine the outcomes of chronic HBV infection. Here we report that CD24 polymorphisms affect the risk and progression of chronic HBV infection. Thus the CD24 P170T allele, which is expressed at a higher level, is associated with an increased risk of chronic HBV infection. Among the chronic HBV patients this allele shows recessive association with more rapid progression to liver cirrhosis and hepatocellular carcinoma in comparison to the P170C allele. In contrast, a dinucleotide deletion at position 1527-1528 (P1527del), which reduces CD24 expression, is associated with a significantly reduced risk of chronic HBV infection. To confirm the role for CD24 in liver carcinogenesis, we compared the size of liver tumor developed in CD24-/- and CD24+/- HBV transgenic mice. Our data demonstrate that targeted mutation of CD24 drastically reduced the sizes of spontaneous liver cancer in the HBV transgenic mice. Conclusion: These data demonstrate that genetic variation of CD24 may be an important determinant for the outcome of chronic HBV infection.