ArticleThe Journal of clinical investigation1998
The C-C chemokine receptor CCR3 participates in stimulation of eosinophil arrest on inflammatory endothelium in shear flow.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 93 citations in OpenAlex.
- Repurposing lapatinib as a triple antagonist of chemokine receptors 3, 4, and 5.Molecular pharmacology · 2025Article
- Epithelial-derived cytokines in the pathogenesis of severe asthma.Frontiers in allergy · 2025Review
- CCR3 Expression in Relation to Delayed Microbleeds in a Rat Model of Large Vessel Occlusion.Journal of experimental neurology · 2024Article
- Expression of Cytokines and Chemokines as Predictors of Stroke Outcomes in Acute Ischemic Stroke.Frontiers in neurology · 2019Article
- Increased expression of chemokine receptors CCR1 and CCR3 in nasal polyps: molecular basis for recruitment of the granulocyte infiltrate.Folia microbiologica · 2013Article
- Transcriptomic analysis of circulating leukocytes reveals novel aspects of the host systemic inflammatory response to sheep scab mites.PloS one · 2012Article
- Up-regulation of CCL11 and CCL26 is associated with activated eosinophils in bullous pemphigoid.Clinical and experimental immunology · 2011Article
- Inflammatory cell migration into the central nervous system: a few new twists on an old tale.Brain pathology (Zurich, Switzerland) · 2007Review
- Eosinophil function in allergic inflammation: from bone marrow to tissue response.Current allergy and asthma reports · 2004Review
- Eosinophil recruitment in type-2 hypersensitivity pulmonary granulomas: source and contribution of monocyte chemotactic protein-3 (CCL7).The American journal of pathology · 2002Article
- Mechanisms of eosinophil recruitment and activation.Current allergy and asthma reports · 2002Review
- New insights into the role of cytokines in asthma.Journal of clinical pathology · 2001Review
- Chemokines: immunology's high impact factors.Nature immunology · 2001Review
- Intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and regulated on activation normal T cell expressed and secreted are expressed by human breast carcinoma cells and support eosinophil adhesion and activation.The American journal of pathology · 2000Article
- Chemokines and asthma: redundancy of function or a coordinated effort?The Journal of clinical investigation · 1999Review
- Genes that regulate eosinophilic inflammation.American journal of human genetics · 1999Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Chemokines are widely hypothesized to stimulate firm adhesion of leukocytes on endothelium in shear flow. Thus far, this has been demonstrated experimentally for exogenously added chemoattractants, but not for those released by endothelium. We found that human umbilical cord endothelial cells (HUVEC) stimulated with TNF-alpha and IFN-gamma secreted eosinophil chemoattractants into the culture supernatant. This material induced transendothelial chemotaxis, stimulated eosinophil binding to purified intercellular adhesion molecule 1, and augmented binding to purified vascular cell adhesion molecule 1 in a 3-min static assay. Chemotaxis and stimulation of adhesion were abrogated completely by the pretreatment of eosinophils with an mAb to the C-C chemokine receptor 3 (CCR3). Eosinophils accumulated efficiently on HUVEC stimulated with TNF-alpha and IFN-gamma in shear flow at 1.5 dyn/cm2. CCR3 mAb slightly but significantly reduced eosinophil arrest and accumulation, by preventing development of firm adhesion by some of the tethered eosinophils, so that they detached within 30 s after the initial tethering. In the presence of mAb to the alpha4 integrin subunit, the effect of CCR3 mAb was more prominent, and approximately half of eosinophil arrest and accumulation was abolished. Inhibition by CCR3 mAb in the presence of beta2 integrin mAb was similar to that in control eosinophils. This is the first evidence that endothelial cell-derived chemokines can activate firm adhesion through alpha4 and beta2 integrins even in the presence of shear flow.
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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.