Document Detail


CD69 limits the severity of cardiomyopathy after autoimmune myocarditis.
MedLine Citation:
PMID:  20855659     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Experimental autoimmune myocarditis (EAM), a mouse model of post-infectious cardiomyopathy, reflects mechanisms of inflammatory cardiomyopathy in humans. EAM is characterized by an infiltration of inflammatory cells into the myocardium that can be followed by myocyte fibrosis, edema, and necrosis, leading to ventricular wall dysfunction and heart failure. Different data indicate that CD69 exerts an important immunoregulatory effect in vivo. However, the possible role of CD69 in autoimmune myocarditis has not been studied. METHODS AND RESULTS: We have explored the role of the leukocyte regulatory molecule CD69 in the inflammation that leads to cardiac dysfunction after myocardial injury in EAM. We have found that after induction of EAM, the draining lymph nodes from CD69-deficient mice developed an exacerbated Th17 inflammatory response, resulting in increases in the numbers of infiltrating leukocytes in the myocardium. In the chronic phase of EAM, transthoracic echocardiography revealed a significantly reduced left ventricular fractional shortening and a decreased ejection fraction in CD69-deficient mice, indicative of an impaired cardiac contractility. This condition was accompanied by a greater extent of myocardial fibrosis, an elevated number of sinus pauses on ECG, and an enhanced ratio of heart weight to body weight in CD69-/- mice. Moreover, both bone marrow transplantation and adoptive transfer of Th17 cells isolated from immunized CD69-/- mice with EAM into naive wild-type recipients reproduced the severity of the disease, demonstrating that CD69 exerts its function within the lymphocyte compartment. CONCLUSION: Our findings indicate that CD69 negatively regulates heart-specific Th17 responses, cardiac inflammation, and heart failure progression in EAM.
Authors:
Aranzazu Cruz-Adalia; Luis Jesús Jiménez-Borreguero; Marta Ramírez-Huesca; Isabel Chico-Calero; Olga Barreiro; Erica López-Conesa; Manuel Fresno; Francisco Sánchez-Madrid; Pilar Martín
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-20
Journal Detail:
Title:  Circulation     Volume:  122     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-05     Completed Date:  2010-10-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1396-404     Citation Subset:  AIM; IM    
Affiliation:
Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Melchor Fernández Almagro, Madrid, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD / genetics
Antigens, Differentiation, T-Lymphocyte / genetics
Autoimmune Diseases / genetics,  immunology,  physiopathology*
Crosses, Genetic
Endomyocardial Fibrosis / immunology,  physiopathology
Female
Flow Cytometry
Humans
Lectins, C-Type / deficiency*,  genetics
Lymph Nodes / cytology,  physiology
Mice
Mice, Inbred BALB C
Mice, Knockout
Myocarditis / genetics,  immunology,  physiopathology*
Myosin Heavy Chains / immunology
Peptide Fragments / immunology
Severity of Illness Index
Spleen / cytology,  physiology
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Antigens, Differentiation, T-Lymphocyte; 0/CD69 antigen; 0/Lectins, C-Type; 0/Myosin Heavy Chains; 0/Peptide Fragments

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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