International Immunology, Vol. 11, No. 1, 1-10,
January 1999
© 1999 Japanese Society for Immunology
Selective eosinophil transendothelial migration triggered by eotaxin via modulation of Mac-1/ICAM-1 and VLA-4/VCAM-1 interactions
1 The Center for Blood Research, Inc. and
2 The Department of Genetics and Pathology, Harvard Medical School. Boston, MA 02115, USA
3 Centro de Investigaciones Biologicas, Madrid 28006, Spain
4 Toronto Hospital, 200 Elizabeth Street, CCRW 1–855, Toronto, Ontario, M5G 2C4, Canada
5 Millennium Pharmaceuticals, Inc. Cambridge, MA 02139, USA
Correspondence to: G.-Q. Jia, Millennium Pharmaceutical Inc., 640 Memorial Drive, Cambridge, MA 02139, USA
We have recently cloned eotaxin, a highly efficacious eosinophilic chemokine involved in the development of lung eosinophilia during allergic inflammatory reactions. To understand more precisely how eotaxin facilitates the specific migration of eosinophils, we have studied which adhesion receptors are essential for eotaxin action both in vivo and in vitro. Experiments using mice genetically deficient in adhesion receptors demonstrated that molecules previously reported to be involved in both leukocyte tethering/rolling (P-selectin and E-selectin) and in sticking/transmigration (ICAM-1 and VCAM-1) are required for eotaxin action in vivo. To further elucidate the mechanism(s) involved in this process, we have used an in vitro transendothelial chemotaxis model. mAb neutralization studies performed in this system suggest that the integrins Mac-1 (CD11b/18), VLA-4 (
4ß1) and LFA-1 (CD11a/18) are involved in the transendothelial chemotaxis of eosinophils to eotaxin. Accordingly, the expression of these integrins on eosinophils is elevated by direct action of this chemokine in a concentration-dependent manner. Taken together, our results suggest that eotaxin-induced eosinophil transendothelial migration in vivo and in vitro relies on Mac-1/ICAM-1 and VLA-4/VCAM-1 interactions, the latter ones becoming more relevant at later time points of the eotaxin-induced recruitment process.
Keywords: chemokine, eotaxin, eosinophil, integrin, transendothelial migration
Transmitting editor: C. Martinez-A
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