摘要
目的通过对JNK/SAPK和p38MAPK信号转导通路在外周血淋巴细胞迁移过程中作用的研究,探讨类风湿关节炎(RA)的发病机制。方法选择20例RA患者,均符合1987年美国风湿病学会推荐的RA分类标准;正常对照20名,为健康体检者。分离出外周血淋巴细胞,应用Western-blot方法检测JNK/SAPK和p38MAPK的表达。结果 RA患者外周血淋巴细胞内p-JNK和p-p38MAPK的表达均高于正常对照组(P<0.05);加入CCL21作用后,正常对照者和RA患者的淋巴细胞表达p-JNK和p-p38MAPK均比CCL21作用前明显增加,且RA患者与正常对照者相比增加更多;而加入抗CCR7抗体后,p-JNK和p-p38MAPK的表达均明显下降(P<0.01)。结论 CCL21/CCR7作为胞外信号分子能够通过激活外周血淋巴细胞的JNK和p38MAPK通路,介导淋巴细胞的迁移,在RA患者淋巴细胞向炎症部位聚集的过程中发挥重要作用,也为控制RA病情的发生发展开辟了新的思路。
To explore the pathogenesis of rheumatoid arthritis（RA）,we investigated the roles of JNK/SAPK and p38MAPK pathways on CCL21/CCR7-mediated peripheral blood lymphocyte chemotaxis in RA patients.Total of 20 RA patients,accorded with the classificatory standard recommended by ACR in 1987,were selected,while 20 healthy individuals were recruited as normal controls.Western blot assays showed that the expressions of JNK and p38MAPK in peripheral blood lymphocytes from RA patients were higher than that from normal controls.Moreover,after adding CCL21,we found the expressions of JNK and p38MAPK increased greatly and the expressions in RA patients increased more highly than that in normal controls.While after anti-CCR7 antibody was added to the samples,the expressions of JNK and p38MAPK decreased significantly.As one of important extracellular signal molecules,CCL21 interacts with CCR7 and mediates lymphocyte migration by activating JNK/SAPK and p38MAPK pathways,thus plays important roles on lymphocytes gathering to inflammatory sites in the patients with RA.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2011年第3期246-249,共4页
Immunological Journal
基金
国家自然科学基金资助项目(30801204)
