B-Cell Immune Responses in Myocarditis: Mechanisms, B-Cell Receptor Repertoire, and Clinical Translation.
- 1Department of Immunology, Center of Immunomolecular Engineering, Zunyi Medical University, Zunyi 563003, China.
Abstract
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⁺ B cells promote persistent inflammation and myocardial fibrosis, whereas IL-10⁺ regulatory B cells (Bregs) confer immune protection by suppressing Th17 responses and maintaining Treg homeostasis. Studies of ICI-associated myocarditis suggest that BCR repertoire features and autoantibody profiles may provide insights into disease-associated immune remodeling. However, the clinical utility of these features as biomarkers remains uncertain, given the lack of standardized assays and sufficiently validated sensitivity, specificity, and reproducibility. In the future, integrating BCR repertoire, multi-omics, and functional subset analyses may improve characterization of disease-associated humoral immune responses and help identify candidate biomarkers for further clinical investigation.
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BibTeX
@article{lin2026bcell,
title = {{B-Cell Immune Responses in Myocarditis: Mechanisms, B-Cell Receptor Repertoire, and Clinical Translation.}},
author = {Xixiong Lin and Xinsheng Yao and Jun Li},
journal = {Cells},
year = {2026},
month = sep,
doi = {10.3390/cells15191734},
url = {https://europepmc.org/article/MED/42882432},
note = {CC BY},
}
RIS
TY - JOUR
TI - B-Cell Immune Responses in Myocarditis: Mechanisms, B-Cell Receptor Repertoire, and Clinical Translation.
AU - Xixiong Lin
AU - Xinsheng Yao
AU - Jun Li
PY - 2026
DA - 2026/09/23
JO - Cells
DO - 10.3390/cells15191734
UR - https://europepmc.org/article/MED/42882432
AB - 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⁺ B cells promote persistent inflammation and myocardial fibrosis, whereas IL-10⁺ regulatory B cells (Bregs) confer immune protection by suppressing Th17 responses and maintaining Treg homeostasis. Studies of ICI-associated myocarditis suggest that BCR repertoire features and autoantibody profiles may provide insights into disease-associated immune remodeling. However, the clinical utility of these features as biomarkers remains uncertain, given the lack of standardized assays and sufficiently validated sensitivity, specificity, and reproducibility. In the future, integrating BCR repertoire, multi-omics, and functional subset analyses may improve characterization of disease-associated humoral immune responses and help identify candidate biomarkers for further clinical investigation.
SN - 2073-4409
ER -