Adhesion of human basophils, eosinophils, and neutrophils to interleukin 1-activated human vascular endothelial cells: contributions of endothelial cell adhesion molecules.

DOI PDF 被引用文献9件
  • B S Bochner
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • F W Luscinskas
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • M A Gimbrone
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • W Newman
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • S A Sterbinsky
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • C P Derse-Anthony
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • D Klunk
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.
  • R P Schleimer
    Division of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224.

書誌事項

公開日
1991-06-01
DOI
  • 10.1084/jem.173.6.1553
公開者
Rockefeller University Press

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説明

<jats:p>Cytokines such as interleukin 1 (IL-1) promote adhesiveness in human umbilical vein endothelial cells for leukocytes including basophils, eosinophils, and neutrophils, and induce expression of adherence molecules including ICAM-1 (intercellular adhesion molecule-1), ELAM-1 (endothelial-leukocyte adhesion molecule-1), and VCAM-1 (vascular cell adhesion molecule-1). In the present study, blocking monoclonal antibodies (mAb) recognizing ICAM-1, ELAM-1, and VCAM-1 have been used to compare their roles in IL-1-induced adhesion of human basophils, eosinophils, and neutrophils. IL-1 treatment of endothelial cell monolayers for 4 hours induced a four- to eight-fold increase in adhesion for each cell type. Treatment of endothelial cells with either anti-ICAM-1 or anti-ELAM-1 mAb inhibited IL-1-induced adherence of each cell type. In contrast, treatment with anti-VCAM-1 mAb inhibited basophil and eosinophil (but not neutrophil) adhesion, and was especially effective in blocking eosinophil adhesion. The effects of these mAb were at least additive. Indirect immunofluorescence and flow cytometry demonstrated expression of VLA-4 alpha (very late activation antigen-4 alpha, a counter-receptor for VCAM-1) on eosinophils and basophils but not on neutrophils. These data document distinct roles for ICAM-1, ELAM-1, and VCAM-1 during basophil, eosinophil, and neutrophil adhesion in vitro, and suggest a novel mechanism for the recruitment of eosinophils and basophils to sites of inflammation in vivo.</jats:p>

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