Increased expression of CCR5 in experimental autoimmune myocarditis and reduced severity induced by anti-CCR5 monoclonal antibody
会议名称：《2007年全国生化与生物技术药物学术年会》
会议日期：2007年
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
摘 要：正We investigated the role of CCR5 in the development of EAM *** fred that CCR5 is important in the induction of EAM and inhibition of CCR5 with monoclonal antibody significantly reduces the severity of ***5 may have the potential to become a new therapy target against autoimmune myocarditis. ABSTRACT:Background Experimental autoimmune myocarditis（EAM）is a T-cell-mediated autoimmune ***5,which is expressed mostly on activated T cells and monocytes /macrophages,are potent chemotactic factors for autoimmune *** investigated the role of CCR5 in the formation of experimental autoimmune *** Expressions of CCR5 and its cognate ligands were assessed by RT-PCR and immunohistochemical ***-cell suspension of splenocytes and whole blood specimens from EAM mice were subjected to flow-cytometry *** investigated the critical role of CCR5 in EAM mice by adoptively transferring CCRS-positive/negative T cells to mice and neutralizing CCR5 with monoclonal antibody to observe the influence on the severity and prevalence of *** We found that CCRS-positive cells predominate in infiltrated inflammatory cells in cardiac tissue of EAM mice and CCR5-positive T cells in peripheral blood increased markedly in EAM mice compared with ***, we demonstrated that the severity of myocarditis was significantly reduced when CCRS-negative T cells from EAM mice were adoptively *** administrated with CCRS-positive T cells,the myocarditis was significantly *** also demonstrated that blockade of CCR5 with monoclonal antibodies significantly reduced severity of myocarditis in EAM *** Overall,these findings indicate that CCR5 is important in the induction of EAM and inhibition of CCR5 with monoclonal antibody significantly reduces the severity of ***5 may have the potential to become a new therapy target against autoimmune myocarditis.