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

@entity1 @entity11502 @entity296 @entity712 @entity19 @entity1184 @entity784 @entity466 @entity5696 @entity6462 @entity4202 @entity37996
BACKGROUND: Limited information exists on the role of B-cell-dependent mechanisms in the progression of @entity712 ( @entity712 ). However, in failing @entity1 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 @entity712 progression using a nonsurgical @entity19 model of @entity296 (CMP). METHODS AND RESULTS: CMP protocol involved the use of @entity6462 and @entity4202 in the drinking water and @entity11502 infusion for 35 days. At day 35, @entity19 were analyzed by cardiac magnetic resonance imaging, gene expression, and histology. @entity19 (12 weeks old) were divided into 4 groups, all in C57BL/6 background: wild-type (WT) CMP; @entity466 ( @entity466 ) CMP (T- and B-cell deficient); @entity37996 (-) CMP (B-cell depleted); and Nude CMP ( @entity784 ), 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 @entity1184 and collagen deposition and a preserved ejection fraction in the @entity37996 (-) CMP group compared to WT CMP. Once @entity466 @entity19 underwent B-cell reconstitution with isolated CMP B-cells, the CMP phenotype was restored. Furthermore, deposition of @entity5696 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 @entity712 resulted in less @entity1184 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 @entity11502 -induced @entity712 model.
