【Abstract】ObjectiveTo investigate the effect of RNA editing enzyme ADAR1 on the function of lymphocyte immune by transferring mouse lymphocytes with plasmid of sense siRNA and by suppressing the expression of ADAR1.
MethodsThe cell strains of human hepatic cellular carcinoma (HCC) were frozen and thawed repeatedly to prepare for tumor soluble antigen. The isolated mouse lymphocytes, which were transferred with antisense siRNA plasmid of ADAR1 and were sensitized with soluble tumor antigen were used as the study group; those which were not transferred but were sensitized were used as the control group. The 3HTdR adulteration experiment was used to test the sensitivity of lymphocytes. The effect of ADAR1 on lymphocyte immunity was detected by lymphocytotoxicity tests.
ResultsThe observation of the isolated lymphocytes implied that the growth cycle of lymphocyte was 10-14 days. The 3HTdR adulteration experiment showed the result was optimal. The number of HCCs decreased significantly for both of the groups compared with those in the blank holes, but the amplitude was much larger in the control group. The expression of ADAR1 in lymphocytes of the study group was significantly lower than that of the control group, which demonstrated that the RNA plasmid of ADAR1 suppressed the expression of ADAR1 in sensitized lymphocytes and the suppressing rate of the control group (87.47±4.62)% was significantly higher than that of study group (53.19±3.95)%. The function of lymphocytes killing targetcells in the study group was significantly inferior to that of control group (P<0.05).
ConclusionRNA editing enzyme ADAR1 may play an important role in mouse cellullar immunologic response and it is possible to attenuate the cellimmune response by depressing the expression of ADAR1.
Citation: KONG Yalin,DOU Kefeng,FENG Quanxin,ZHANG Hongtao,LI Jun,ZHANG Fuqin,ZHAO Qingchuan.. Function of RNA Editing Enzyme ADAR1 in Cellullar Immunologic Response in Mouse. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2006, 13(3): 279-282. doi: Copy