VCAM-1
细胞粘附分子
嗜酸性粒细胞
粘附
细胞粘附
可溶性细胞粘附分子
ICAM-1
嗜碱性粒细胞
内皮
细胞生物学
免疫学
内皮干细胞
细胞间粘附分子-1
生物
分子生物学
化学
抗体
生物化学
体外
内分泌学
免疫球蛋白E
哮喘
有机化学
作者
Robert P. Schleimer,Sherry A. Sterbinsky,Jean‐Pierre Kaiser,Carol A. Bickel,D A Klunk,K. Tomioka,Walter Newman,Francis W. Luscinskas,Michael A. Gimbrone,Bradley W. McIntyre
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:1992-02-15
卷期号:148 (4): 1086-1092
被引量:719
标识
DOI:10.4049/jimmunol.148.4.1086
摘要
Abstract The present studies were performed to explore potentially selective mechanisms of leukocyte adhesion in an attempt to understand how preferential recruitment of eosinophils and basophils might occur during allergic and other inflammatory reactions. Stimulation of human vascular endothelial cells for 24 h with IL-4 (30 to 1,000 U/ml) induced adhesion for eosinophils (up to approximately four-fold of control) and basophils (up to approximately twofold of control) but not neutrophils (less than 125% of control). Analysis of endothelial expression of adhesion molecules by flow cytometry revealed that IL-4 treatment induced vascular cell adhesion molecule-1 (VCAM-1) expression without significantly affecting the expression of other adhesion molecules, namely endothelial-leukocyte adhesion molecule-1 (ELAM-1) or intercellular adhesion molecule-1 (ICAM-1). The concentration-response curve for IL-4-induced VCAM-1 expression paralleled that for adhesion. Endothelial cells stimulated with IL-4 expressed adhesive properties for eosinophils by 3 h; the response increased steadily during a 24-h time course study. Eosinophils and basophils adhered to plates coated with a recombinant form of VCAM-1. This adhesion was blocked with antibodies to VCAM-1 but not ELAM-1. mAb directed against either VCAM-1 or VLA-4 inhibited (by approximately 75%) the binding of eosinophils and basophils to IL-4-stimulated endothelial cells. Because VLA-4 and VCAM-1 have been demonstrated to bind to each other in other adhesion systems, these results suggest that IL-4 stimulates eosinophil and basophil adhesion by inducing endothelial cell expression of VCAM-1 which binds to eosinophil and basophil VLA-4. The lack of expression of VLA-4 on neutrophils and the failure of IL-4 to stimulate neutrophil adherence support this conclusion. It is proposed that local release of IL-4 in vivo in allergic diseases or after experimental allergen challenge may partly explain the enrichment of eosinophils and basophils (vs neutrophils) observed in these situations.
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