ArticleCell adhesion & migration
P-selectin cross-links PSGL-1 and enhances neutrophil adhesion to fibrinogen and ICAM-1 in a Src kinase-dependent, but GPCR-independent mechanism.
Article in Cell adhesion & migration. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Platelet-leucocyte interactions drive MMP-mediated tissue damage in tuberculosis.PLoS pathogens · 2026Article
- Review
- Dengue virus infection: how platelet-leukocyte crosstalk shapes thrombotic events and inflammation.Molecular biology reports · 2025Review
- A pair of promising immune checkpoints PSGL-1 and VISTA from immunotolerance to immunotherapy.Biomarker research · 2024Review
- Chemokine binding to PSGL-1 is controlled by O-glycosylation and tyrosine sulfation.Cell chemical biology · 2023Article
- Platelet and Megakaryocyte Roles in Innate and Adaptive Immunity.Circulation research · 2022Review
- Endothelial cells, neutrophils and platelets: getting to the bottom of an inflammatory triangle.Open biology · 2020Review
- Platelet P-selectin initiates cross-presentation and dendritic cell differentiation in blood monocytes.Science advances · 2020Article
- Platelet-Adherent Leukocytes Associated With Cutaneous Cross-Reactive Hypersensitivity to Nonsteroidal Anti-Inflammatory Drugs.Frontiers in pharmacology · 2020Article
- The P-selectin and PSGL-1 axis accelerates atherosclerosis via activation of dendritic cells by the TLR4 signaling pathway.Cell death & disease · 2019Article
- Integrin α4β7 switches its ligand specificity via distinct conformer-specific activation.The Journal of cell biology · 2018Article
- Integration of multi-omics data and deep phenotyping enables prediction of cytokine responses.Nature immunology · 2018Article
- Alternatively-Activated Macrophages Upregulate Mesothelial Expression of P-Selectin to Enhance Adhesion of Ovarian Cancer Cells.Cancer research · 2018Article
- Targeting the PSGL-1 pathway for immune modulation.Immunotherapy · 2017Article
- Article
- PSGL-1: A New Player in the Immune Checkpoint Landscape.Trends in immunology · 2017Review
- Technical Advance: Changes in neutrophil migration patterns upon contact with platelets in a microfluidic assay.Journal of leukocyte biology · 2017Article
- Leukocyte transendothelial migration: A local affair.Small GTPases · 2017Review
- Platelet-neutrophil interactions under thromboinflammatory conditions.Cellular and molecular life sciences : CMLS · 2015Review
- Platelets and Their Interactions with Other Immune Cells.Comprehensive Physiology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Endothelial and platelet P-selectin (CD62P) and leukocyte integrin alpha(M)beta(2) (CD11bCD18, Mac-1) are cell adhesion molecules essential for host defense and innate immunity. Upon inflammatory challenges, P-selectin binds to PSGL-1 (P-selectin glycoprotein ligand-1, CD162) to mediate neutrophil rolling, during which integrins become activated by extracellular stimuli for their firm adhesion in a G-protein coupled receptor (GPCR)-dependent mechanism. Here we show that cross-linking of PSGL-1 by dimeric or multimeric forms of platelet P-selectin, P-selectin receptor-globulin, anti-PSGL-1 mAb and its F(ab')2 induced adhesion of human neutrophils to fibrinogen (Fg) and intercellular cell adhesion molecule-1 (ICAM-1, CD54) and triggered a moderate clustering of alpha(M)beta(2), but monomeric forms of soluble P-selectin and anti-PSGL-1 Fab did not. Interestingly, P-selectin did not induce a detectable interleukine-8 (IL-8) secretion (<0.1 ng/ml) in 30 minutes, whereas a high concentration of IL-8 (>50 ng/ml) was required to increase neutrophil adhesion to Fg. P-selectin-induced neutrophil adhesion was significantly inhibited by PP2 (a Src kinase inhibitor), but not by pertussis toxin (PTX; a GPCR inhibitor). Activated platelets also increased neutrophil binding to fibrinogen and triggered tyrosine phosphorylation of cellular proteins. Our results indicate that P-selectin-induced integrin activation (Src kinase-dependent) is distinct from that elicited by cytokines, chemokines, chemoattractants (GPCR-dependent), suggesting that these two signal transduction pathways may cooperate for maximal activation of leukocyte integrins.
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Registered trials
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.