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Cited by 898

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of asthma

Wegner, Craig D., Gundel, Robert H., Reilly, Patricia, Haynes, Nancy, Letts, L. Gordon, Rothlein, Robert·1990·Science

Abstract

Airway eosinophilia, epithelial desquamation, and hyperresponsiveness are characteristics of the airway inflammation underlying bronchial asthma. The contribution of intercellular adhesion molecule-1 (ICAM-1) to eosinophil migration and airway responsiveness was studied. ICAM-1 partially mediated eosinophil adhesion to endothelium in vitro and was upregulated on inflamed bronchial endothelium in vivo. ICAM-1 expression was also upregulated on inflamed airway epithelium in vitro and in vivo. In a primate model of asthma, a monoclonal antibody to ICAM-1 attenuated airway eosinophilia and hyperresponsiveness. Thus, antagonism of ICAM-1 may provide a therapeutic approach to reducing airway inflammation, hyperresponsiveness, and asthma symptoms.

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Crossref · 10.1126/science.1967851

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Metadata

Authors
Wegner, C. D., Gundel, R. H., Reilly, P., Haynes, N., Letts, L. G., & Rothlein, R.
Venue
Science
Published
1990-01-26
Volume
247
Issue
4941
Pages
456-459
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2015037737
Cited by
898
References
1
FWCI
58.78
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of asthma. https://app.cochat.ai/papers/10.1126/science.1967851
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Wegner, C. D., Gundel, R. H., Reilly, P., Haynes, N., Letts, L. G., & Rothlein, R. (1990). Intercellular Adhesion Molecule-1 (ICAM-1) in the Pathogenesis of asthma. Science. https://doi.org/10.1126/science.1967851

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.