The role of B cells in heart failure and implications for future immunomodulatory treatment strategies.

Gerardo García‐Rivas,Elena Cristina Castillo,José Luis Maravillas‐Montero,Guillermo Torre‐Amione,Alejandro Torres‐Quintanilla,Marion Brunck,Adrian M Gonzalez‐Gil,Leticia Elizondo‐Montemayor

doi:10.1002/ehf2.12744

Abstract

Despite numerous demonstrations that the immune system is activated in heart failure, negatively affecting patients' outcomes, no definitive treatment strategy exists directed to modulate the immune system. In this review, we present the evidence that B cells contribute to the development of hypertrophy, inflammation, and maladaptive tissue remodelling. B cells produce antibodies that interfere with cardiomyocyte function, which culminates as the result of recruitment and activation of a variety of innate and structural cell populations, including neutrophils, macrophages, fibroblasts, and T cells. As B cells appear as active players in heart failure, we propose here novel immunomodulatory therapeutic strategies that target B cells and their products.

Highlights

Heart failure (HF) is accompanied by a systemic pro-inflammatory state,[1] in which both the innate and adaptive immune system participate.[2,3] Despite mounting evidence linking inflammation and HF, specific immunomodulatory therapies for HF have not been successfully developed
This is explained in part because not all the components of the immune system have been thoroughly investigated in the context of HF, as is the specific role that each immune cell plays in the heart
We present current evidence of the role of B cells in adverse cardiac remodelling, highlighting that this role is independent of aetiology, and introduce our ongoing investigations into novel immunomodulatory therapeutic strategies that target B cells and their products

Summary

Introduction

Heart failure (HF) is accompanied by a systemic pro-inflammatory state,[1] in which both the innate and adaptive immune system participate.[2,3] Despite mounting evidence linking inflammation and HF, specific immunomodulatory therapies for HF have not been successfully developed. Despite mounting evidence linking inflammation and HF, specific immunomodulatory therapies for HF have not been successfully developed. This is explained in part because not all the components of the immune system have been thoroughly investigated in the context of HF, as is the specific role that each immune cell plays in the heart. Germane to this discussion is the fact that the accumulated evidence shows that B cells, both directly (by secreting antibodies) and indirectly (by antigen presentation and cytokines/chemokines secretion), play an essential role in the progression of HF. Antibody-mediated contribution to cardiac injury includes, on the one hand, direct consequences of anti-cardiac antibodies binding to target cells and, on the other hand, the activation of the complement system following the formation of antigen–antibody complexes

García-Rivas et al

Findings

Conclusions