ArticleCellular & molecular immunology2024
Neutrophils disrupt B-1a cell homeostasis by targeting Siglec-G to exacerbate sepsis.
Article in Cellular & molecular immunology, 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.
- Role of DLL4 in Neutrophil Aging and Impaired Clearance in Sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Cell-based drug delivery for combating bacteria: focus on refractory infections.Journal of nanobiotechnology · 2026Review
- Review
- Neutrophil Irgm1 ameliorates sepsis-induced myocardial dysfunction by promoting Alox15 degradation.Redox biology · 2026Article
- Nanotherapeutic Macrophage-Neuro Reprogramming Through Immunometabolic Crosstalk Mitigates Sepsis-Induced Lung Injury and Neurologic Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A decoy oligodeoxynucleotide favors the differentiation of CpG ODN-induced B cells into IL-10-producing Breg-like cells over plasma cells by restoring IRF4/IRF8 imbalance.Cellular and molecular life sciences : CMLS · 2026Article
- Immune-inflammatory endotypes of chronic rhinosinusitis: from epithelial alarmins to personalized therapy.Frontiers in immunology · 2026Review
- Neutrophil in sepsis: functional aberration and regulated cell death.Frontiers in immunology · 2026Review
- B-1a cells mitigate radiation injury by protecting intestinal barrier integrity.Frontiers in immunology · 2026Article
- DLL4+ neutrophils promote Notch1-mediated endothelial PANoptosis to exacerbate acute lung injury in sepsis.The Journal of clinical investigation · 2025Article
- Gut-primed neutrophils activate Kupffer cells to promote hepatic injury in mouse sepsis.Nature communications · 2025Article
- Critical Role of IL1R2-ENO1 Interaction in Inhibiting Glycolysis-Mediated Pyroptosis for Protection Against Lethal Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CircIRAK3 Promotes Neutrophil Extracellular Trap Formation by Improving the Stability of ELANE mRNA in Sepsis.Inflammation · 2025Article
- CD300ld promotes neutrophil bacterial phagocytosis in sepsis.Journal of leukocyte biology · 2025Article
- The Infectivity and Pathogenicity Characteristics of a Recombinant Porcine Epidemic Diarrhea Virus, CHFJFQ.Viruses · 2025Article
- A novel molecule targeting neutrophil-mediated B-1a cell trogocytosis attenuates sepsis-induced acute lung injury.Frontiers in immunology · 2025Article
- Siglec-G Suppresses CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
B-1a cells, an innate-like cell population, are crucial for pathogen defense and the regulation of inflammation through their release of natural IgM and IL-10. In sepsis, B-1a cell numbers are decreased in the peritoneal cavity as they robustly migrate to the spleen. Within the spleen, migrating B-1a cells differentiate into plasma cells, leading to alterations in their original phenotype and functionality. We discovered a key player, sialic acid-binding immunoglobulin-like lectin-G (Siglec-G), which is expressed predominantly on B-1a cells and negatively regulates B-1a cell migration to maintain homeostasis. Siglec-G interacts with CXCR4/CXCL12 to modulate B-1a cell migration. Neutrophils aid B-1a cell migration via neutrophil elastase (NE)-mediated Siglec-G cleavage. Human studies revealed increased NE expression in septic patients. We identified an NE cleavage sequence in silico, leading to the discovery of a decoy peptide that protects Siglec-G, preserves peritoneal B-1a cells, reduces inflammation, and enhances sepsis survival. The role of Siglec-G in inhibiting B-1a cell migration to maintain their inherent phenotype and function is compromised by NE in sepsis, offering valuable insights into B-1a cell homeostasis. Employing a small decoy peptide to prevent NE-mediated Siglec-G cleavage has emerged as a promising strategy to sustain peritoneal B-1a cell homeostasis, alleviate inflammation, and ultimately improve outcomes in sepsis patients.
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Registered trials
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