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小鼠GITRL蛋白对Th17细胞的影响及其在小鼠CIA发病中的作用 |
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hology of mouse joints showed that there were significant cell infiltration and synovium hyperplasy within the articular space in the CTL-CIA group,but there were more serious inflammatory changes in the GITRL-CIA group,including pannus formation and artilage damage, besides significant cell infiltration and synovium hyperplasy.While CTL-CIA and CIA groups showed no difference in their clinical scores and pathology change.Compared with the CIA group(2.49×105±9.07×104) and CTL-CIA group(2.07×105±7.01×104),the number of Th17 cells in draining lymph nodes of the GITRL-group increased significantly(2.30×106±9.11×105)(p<0.05).Compared with the CIA group(8.93±3.20 pg/ml) and CTL-CIA group(8.15±2.56 pg/ml),the level of IL-17 in serum of the GITRL-CIA group increased significantly (17.59±3.46pg/ml)(p<0.05).Conclusions:(1) The mGITRL fusion protein was expressed and purified successfully.Rabbit anti-mouse GITRL polyclonal antibody was prepared.(2) Mouse GITRL can increase the percentage of Th17 cells and the production of IL-17 in vitro,and it showed a dose-dependent relationship.(3) Mouse GITRL can raise the frequency of Th17 cells in spleens and the level of IL-17 in serum in vivo,with an increase level of RORγt in spleens.(4) Our results suggested that mouse GITRL can exaberbate the development of collagen-induced arthritis in mice,which may correlate with the increasing number of Th17 cells in draining lymph nodes and the level of IL- 17 in serum.
【Key words】 GITRL; Th17 cells; RORγt; IL-17; CIA; mice Feldmann M, Brennan FM, Maini RN. Rheumatoid arthritis[J].Cell,1996,85(3):307-310. [2]. Vassalli P. The pathophysiology of tumor necrosis factors[J].Annual Review of Immunology,1992,10:411-452. [3]. Matthys P;Hatse S;Vermeire k,et al. AMD3100,a potent and specific an-tagonist of the stromal cell-derivedfactor-1 chemokine receptor cxcr4,in
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