The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/4/1493/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 8, April 21, 1997 1493-1498

Brief Definitive Reports

Anti-CD43 Inhibition of T Cell Homing

Leslie M. McEvoy*,{ddagger}, Hailing Sun*,{ddagger}, John G. Frelinger§, and Eugene C. Butcher*,{ddagger}

From the * Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, Stanford, California 94305; {ddagger} Center for Molecular Biology and Medicine, Veterans Affairs Health Care System, Palo Alto, California 94304; and § Department of Microbiology and Immunology, The Cancer Center of the University of Rochester School of Medicine and Dentistry, Rochester, New York 14642

The homing of lymphocytes from the blood is controlled by specialized processes of lymphocyte–endothelial cell interaction. Interference with these processes offers the potential to manipulate lymphocyte traffic, and thus to modulate normal and pathologic immune and inflammatory responses. We selected antilymphocyte monoclonal antibodies (mAbs) for inhibition of lymphocyte binding in vitro to lymph node high endothelial venules (HEV), specialized vessels that support lymphocyte recruitment into lymph nodes. mAb L11 blocks T cell binding to lymph node and Peyer's patch HEV and inhibits T cell extravasation from the blood into organized secondary lymphoid tissues. In contrast, L11 has no effect on lymphocyte binding to purified vascular ligands for L-selectin, {alpha}4β7, or LFA-1, suggesting that it inhibits by a novel mechanism. The L11 antigen is CD43, a sialomucin implicated in vitro in regulation of lymphocyte activation, whose expression is often dysregulated in the Wiskott-Aldrich syndrome. CD43 represents a novel target for experimental and therapeutic manipulation of lymphocyte traffic and may help regulate T cell distribution in vivo.

Address correspondence to Dr. Leslie M. McEvoy, Department of Pathology, L235, Stanford University, Stanford, CA 94305.

L.M. McEvoy was a Senior Fellow of the American Heart Association, California Division, and the National Multiple Sclerosis Society during part of this work. H. Sun is supported by a predoctoral award by the National Cancer Institute. This work was supported by grant AI37319 from the National Institutes of Health and the Core Facilities of the Stanford Digestive Disease Center under DK38707.


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