The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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Published online 2 July 2001. doi:10.1084/jem.194.1.107
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© The Rockefeller University Press, 0022-1007/2001/7/107/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 1, July 2, 2001 107-112


Brief Definitive Report

This article was retracted on September 29, 2003

The Epithelial Cellular Adhesion Molecule (Ep-CAM) Is a Ligand for the Leukocyte-associated Immunoglobulin-like Receptor (LAIR)

Linde Meyaarda, Anne-Renée van der Vuurst de Vriesa, Talitha de Ruitera, Lewis L. Lanierc, Joseph H. Phillipsb, and Hans Cleversa
a Department of Immunology, University Medical Center, 3584 CX Utrecht, Netherlands
b Department of Immunobiology, DNAX Research Institute, Palo Alto, CA 94304
c Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, CA 94304

Correspondence to: Linde Meyaard, Department of Immunology, University Medical Center, Heidelberglaan 100, Rm. F03.821, 3584 CX Utrecht, Netherlands. Tel:31-30-2507674 Fax:31-30-2517107 E-mail:l.meyaard{at}lab.azu.nl.

Human leukocyte-associated immunoglobulin-like receptor (LAIR)-1 is expressed on many cells of the immune system and is predicted to mediate inhibitory functions based on the presence of immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in its cytoplasmic domain. Although the role of LAIR-1 in the regulation of immune responses in vivo is unknown, LAIR-1 cross-linking by monoclonal antibody inhibits various immune cell functions in vitro. Here, we identify the coloncarcinoma-associated epithelial cellular adhesion molecule (Ep-CAM) as a ligand for LAIR-1 and LAIR-2, a related soluble LAIR-1 family member. Ep-CAM interacts with the LAIR molecules through its first epidermal growth factor domain; Ep-CAM–specific antibodies can abrogate the binding. Intraepithelial T lymphocytes express LAIR-1 and thus may interact with Ep-CAM present on human intestinal epithelium. We propose that LAIR-1–Ep-CAM interaction may contribute to mucosal tolerance and that LAIR-2 possibly modulates this function.

Key Words: ITIM, colon carcinoma, inhibitory receptor, intraepithelial lymphocytes, mucosal tolerance


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