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Research Article Free access | 10.1172/JCI113463

Adherence of human basophils to cultured umbilical vein endothelial cells.

B S Bochner, P T Peachell, K E Brown, and R P Schleimer

Department of Medicine, Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, Maryland 21239.

Find articles by Bochner, B. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, Maryland 21239.

Find articles by Peachell, P. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, Maryland 21239.

Find articles by Brown, K. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, Maryland 21239.

Find articles by Schleimer, R. in: PubMed | Google Scholar

Published May 1, 1988 - More info

Published in Volume 81, Issue 5 on May 1, 1988
J Clin Invest. 1988;81(5):1355–1364. https://doi.org/10.1172/JCI113463.
© 1988 The American Society for Clinical Investigation
Published May 1, 1988 - Version history
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Abstract

The mechanism by which circulating human basophils adhere to vascular endothelium and migrate to sites of allergic reactions is unknown. Agents have been identified which stimulate the adherence of purified basophils to cultured human umbilical vein vascular endothelial cells (HuVEC). Treatment of HuVEC with interleukin 1, tumor necrosis factor (TNF), bacterial endotoxin, and 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in time and dose-dependent increases of adhesiveness for basophils. Coincubation of basophils and HuVEC for 10 min with C5a, formyl-methionyl-leucyl-phenylalanine, the calcium ionophore A23187, platelet-activating factor, TNF, and TPA also resulted in significant dose-dependent increases in basophil adherence; this effect resulted from activation of the basophil. Adherence of basophils to HuVEC was time and temperature dependent, required divalent cations, and was unaffected by glucocorticoids. Monoclonal antibody 60.3, directed against the beta-subunit of the leukocyte adherence complex CD18, inhibited the binding of basophils to HuVEC. Adherence of basophils to vascular endothelium may be important in initiating basophil infiltrates in vivo.

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