Neutrophil migration in infection and wound repair: going forward in reverse

2016/05/27 by Sofía de Oliveira, Sofia de Oliveira, Emily E. Rosowski +1 · 4 citations
Immunology and Microbiology · Medicine · #Cell Adhesion Molecules Research #Immune Response and Inflammation #Neutrophil, Myeloperoxidase and Oxidative Mechanisms

paper · doi:10.1038/nri.2016.49

crossref issued 2016/05/27 · crossref published 2016/05/27 · crossref published-online 2016/05/27 · openalex publication_date 2016/05/27 · crossref created 2016/05/27 · crossref published-print 2016/06/01 · crossref deposited 2023/05/23 · openalex created_date 2025/10/10 · crossref indexed 2026/07/22 · openalex updated_date 2026/08/01

Citations

• Neutrophil gelatinase B potentiates interleukin-8 tenfold by aminoterminal processing, whereas it degrades CTAP-III, PF-4, and GRO-α and leaves RANTES and MCP-2 intact
• Resolution phase lipid mediators of inflammation: agonists of resolution
• CD24-Siglec G/10 discriminates danger- from pathogen-associated molecular patterns
• N-Formyl peptides drive mitochondrial damage associated molecular pattern induced neutrophil activation through ERK1/2 and P38 MAP kinase signalling pathways
• CD24 and Siglec-10 Selectively Repress Tissue Damage–Induced Immune Responses

Cited by

• Decoding the chemotactic signal
• Toll-like receptors in immunity and inflammatory diseases: Past, present, and future
• MCV-miR-M1 Targets the Host-Cell Immune Response Resulting in the Attenuation of Neutrophil Chemotaxis
• Chemotaxis [wikipedia]