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Background  Limited information exists on the role of B‐cell‐dependent mechanisms in the progression of heart failure ( HF ). However, in failing human myocardium, there is evidence of deposition of activated complement components as well as anticardiac antibodies. We aimed to determine the contribution of B‐cells in  HF  progression using a nonsurgical mouse model of nonischemic cardiomyopathy ( CMP ).    Methods and Results   CMP  protocol involved the use of  l ‐ NAME  and NaCl in the drinking water and angiotensin‐ II  infusion for 35 days. At day 35, mice were analyzed by cardiac magnetic resonance imaging, gene expression, and histology. Mice (12 weeks old) were divided into 4 groups, all in C57 BL /6 background: wild‐type ( WT )  CMP ; severe combined immunodeficiency ( SCID )  CMP  (T‐ and B‐cell deficient);  CD 22 −   CMP  (B‐cell depleted); and Nude  CMP  (T‐cell deficient), with their respective controls. We performed B‐cell depletion and reconstitution protocols. The protective effect of B‐cell depletion was demonstrated by a significant reduction of cell hypertrophy and collagen deposition and a preserved ejection fraction in the  CD 22 −   CMP  group compared to  WT CMP . Once  SCID  mice underwent B‐cell reconstitution with isolated  CMP  B‐cells, the  CMP  phenotype was restored. Furthermore, deposition of IgG3 and apoptosis in the myocardium follows the development of  CMP ; in addition, in vitro studies demonstrated that activated B‐cells stimulate collagen production by cardiac fibroblasts.    Conclusions  The absence of B‐cells in this model of  HF  resulted in less hypertrophy and collagen deposition, preservation of left ventricular function, and, in association with these changes, a reduction in expression of proinflammatory cytokines, immunoglobulin G deposition, and apoptosis in the myocardium. Taken together, these data suggest that B‐cells play a contributory role in an angiotensin‐ II ‐induced  HF  model.

journal of the american heart association

Full Expression of Cardiomyopathy Is Partly Dependent on B‐Cells: A Pathway That Involves Cytokine Activation, Immunoglobulin Deposition, and Activation of Apoptosis