| Increased expression of CCR5 in experimental autoimmune myocarditis and reduced severity induced by anti-CCR5 monoclonal antibody. | |
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MedLine Citation:
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PMID: 17362985 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Experimental autoimmune myocarditis (EAM) is a T-cell-mediated autoimmune disease. CCR5, which is expressed mostly on activated T cells and monocytes/macrophages, are potent chemotactic factors for autoimmune myocarditis. We investigated the role of CCR5 in the formation of experimental autoimmune myocarditis. Expression of CCR5 and its cognate ligands was assessed by RT-PCR and immunohistochemical analysis. Single-cell suspension of splenocytes and whole blood specimens from EAM mice were subjected to flow-cytometry analysis. We investigated the critical role of CCR5 in EAM mice by adoptively transferring CCR5-positive/negative T cells to mice and by neutralizing CCR5 with monoclonal antibody to observe the influence on the severity and prevalence of myocarditis. In this report, we found that CCR5-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 controls. Moreover, we demonstrated that the severity of myocarditis was significantly reduced when CCR5-negative T cells from EAM mice were adoptively transferred. When administrated with CCR5-positive T cells, the myocarditis was significantly aggravated. We also demonstrated that blockade of CCR5 with monoclonal antibodies significantly reduced severity of myocarditis in EAM mice. 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 myocarditis. CCR5 may have the potential to become a new therapy target against autoimmune myocarditis. |
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Authors:
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Xuelian Gong; Hao Feng; Shuying Zhang; Yizhi Yu; Jianzhong Li; Jvrong Wang; Baoyu Guo |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-02-11 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 42 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2007 Apr |
Date Detail:
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Created Date: 2007-04-09 Completed Date: 2007-06-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 781-91 Citation Subset: IM |
Affiliation:
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Department of Biochemical Pharmacy, School of Pharmacy, Second Military Medical University, Shanghai 200433, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adoptive Transfer Animals Antibodies, Monoclonal / therapeutic use* Autoimmune Diseases / etiology, immunology, therapy* Chemotaxis, Leukocyte Cytokines / metabolism Enzyme-Linked Immunosorbent Assay Female Lymphocyte Activation Mice Mice, Inbred BALB C Mice, SCID Myocarditis / etiology, immunology, therapy* RNA, Messenger / genetics, metabolism Receptors, CCR5 / antagonists & inhibitors*, genetics, metabolism* T-Lymphocytes Th1 Cells / immunology, metabolism, pathology Th2 Cells / immunology, metabolism, pathology |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Monoclonal; 0/Cytokines; 0/RNA, Messenger; 0/Receptors, CCR5 |
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