RT Journal Article
T1 CD69 Limits the Severity of Cardiomyopathy After Autoimmune Myocarditis
A1 Cruz Adalia, Aranzazu
A1 Jiménez Borreguero, Luis Jesús
A1 Ramírez Huesca, Marta
A1 Chico Calero, Isabel
A1 Barreiro, Olga
A1 López Conesa, Erica
A1 Fresno, Manuel
A1 Sánchez Madrid, Francisco
A1 Martín, Pilar
AB 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.
PB Lippincott, Williams & Wilkins
SN 0009-7322
SN 1524-4539
YR 2010
FD 2010-10-05
LK https://hdl.handle.net/20.500.14352/97205
UL https://hdl.handle.net/20.500.14352/97205
LA eng
NO Cruz-Adalia A, Jiménez-Borreguero LJ, Ramírez-Huesca M, Chico-Calero I, Barreiro O, López-Conesa E, Fresno M, Sánchez-Madrid F, Martín P. CD69 limits the severity of cardiomyopathy after autoimmune myocarditis. Circulation. 2010 Oct 5;122(14):1396-404. doi: 10.1161/CIRCULATIONAHA.110.952820
NO Ministerio de Ciencia e Innovacion
DS Docta Complutense
RD 5 abr 2025