B-Cell Immune Responses in Myocarditis: Mechanisms, B-Cell Receptor Repertoire, and Clinical Translation.

Myocarditis is an inflammatory myocardial disease induced by infection, autoimmunity, or immune checkpoint inhibitor (ICI) therapy. Its immunopathogenesis has long been attributed primarily to T-cell-mediated cellular immunity. Increasing evidence now indicates that B cells contribute to the initiation, persistence, and myocardial remodeling of myocarditis not only as a source of autoantibodies, but also through antigen presentation, cytokine secretion, and immunoregulatory crosstalk. The emergence of single-cell sequencing and B-cell receptor (BCR) repertoire sequencing has begun to reveal B-cell clonal expansion, immunoglobulin class switching, and dynamic shifts in functional subsets, offering a new window into humoral immune responses in myocarditis. This review synthesizes current evidence on BCR repertoire remodeling, autoantibody-mediated myocardial injury, functional heterogeneity among B-cell subsets, and the clinical translation of these findings. B cells can mediate myocardial damage through autoantibodies against adenine nucleotide translocator (ANT), cardiac myosin, and acetylcholine receptor (AChR), and their pathogenic effects depend on immunoregulatory networks such as Th17/IL-17 signaling and autophagy. Notably, B cells are functionally heterogeneous, TNF-α