ArticleJCI insight2024
B cell subsets contribute to myocardial protection by inducing neutrophil apoptosis after ischemia and reperfusion.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- CD8+ regulatory T cells shorten neutrophil lifespan to reduce hemorrhagic transformation after ischemic stroke.The Journal of clinical investigation · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Unraveling the regulatory role of intercellular communication in intestinal immune cells mediated by H₂ in sepsis recovery through single-cell RNA sequencing.Journal of translational medicine · 2026Article
- Nomogram based on quantitative lung CT features to identify cardiovascular disease in chronic obstructive pulmonary disease and predict prognosis.BMC medical imaging · 2026Article
- KLF2 Promotes Neutrophil Apoptosis in Mice with Myocardial ischemia-reperfusion Injury by Upregulating Notch1.Cell biochemistry and biophysics · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Breakthroughs of ultrasound-targeted microbubble destruction in treating myocardial ischemia-reperfusion injury: from angiogenesis regulation to precise inflammation suppression.Drug delivery · 2025Review
- Chemokine-receptor-guided B-cell immunity in cardiovascular disease.Basic research in cardiology · 2025Review
- B cells in non-lymphoid tissues.Nature reviews. Immunology · 2025Review
- Sex differences in the chronic autoimmune response to myocardial infarction.Clinical science (London, England : 1979) · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- CT-Based radiomics nomogram of lung and mediastinal features to identify cardiovascular disease in chronic obstructive pulmonary disease: a multicenter study.BMC pulmonary medicine · 2025Article
- The effect of TIM1Cell death & disease · 2025Article
- A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Lymphocyte Subset Imbalance in Cardiometabolic Diseases: Are T Cells the Missing Link?International journal of molecular sciences · 2025Review
- Hematopoietic effects of Fufang E'jiao Jiang revealed by microbiome, metabolome and transcriptome analyses: a multi-omics strategy.Frontiers in immunology · 2025Article
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A robust, sterile inflammation underlies myocardial ischemia and reperfusion injury (MIRI). Several subsets of B cells possess the immunoregulatory capacity that limits tissue damage, yet the role of B cells in MIRI remains elusive. Here, we sought to elucidate the contribution of B cells to MIRI by transient ligation of the left anterior descending coronary artery in B cell-depleted or -deficient mice. Following ischemia and reperfusion (I/R), regulatory B cells are rapidly recruited to the heart. B cell-depleted or -deficient mice exhibited exacerbated tissue damage, adverse cardiac remodeling, and an augmented inflammatory response after I/R. Rescue and chimeric experiments indicated that the cardioprotective effect of B cells was not solely dependent on IL-10. Coculture experiments demonstrated that B cells induced neutrophil apoptosis through contact-dependent interactions, subsequently promoting reparative macrophage polarization by facilitating the phagocytosis of neutrophils by macrophages. The in vivo cardioprotective effect of B cells was undetectable in the absence of neutrophils after I/R. Mechanistically, ligand-receptor imputation identified FCER2A as a potential mediator of interactions between B cells and neutrophils. Blocking FCER2A on B cells resulted in a reduction in the percentage of apoptotic neutrophils, contributing to the deterioration of cardiac remodeling. Our findings unveil a potential cardioprotective role of B cells in MIRI through mechanisms involving FCER2A, neutrophils, and macrophages.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.