THE EFFECT OF FCγ RECEPTOR ON THE PATHOGENESIS OF GRAVES' DISEASE

摘要

Objective To explore the roles of Fcγ receptor in the pathogenesis of Graves'' disease. Methods Feγ receptor gene knockout mice(Fcγ R KO mice) which were rooted in C57BL/6 mice and wild type C57BL/6 mice were immunized by hTSH receptor expressing cells (DAP3. WT). 1-2 X 10~7 DAP3. WT cells were peritoneally injected into mice every two weeks for a total of six times. Two weeks after final immunization, mice were killed for measurement of total thyroxine, TRAb and pathological examination. Results The thyroxine level of the immunized Fcγ receptor gene knockout mice was significantly lower than that of the immunized wild type control mice (2.2 ± 0.31 vs. 3.32 ± 0.59 g • dL~(-1), P < 0.05), but there was no significant difference between immunized Fcγ R KO mice and non-immunized wild type control group. The TRAb levels of the immunized Fγ R KO mice significantly increased compared to those of the immunized wild type mice (21.75 ± 8.21 vs. 14.11 ± 6.21, P < 0.05). The lymphocyte cells infiltration and destruction of thyroid follicles were found in the thyroid gland of the immunized Fcγ R KO mice. Conclusion These results suggest that Fcγ receptor may be involved in the pathogenesis of Graves'' disease.