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Lymphocyte Biology Section, Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women’s Hospital, and
Combined Program in Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115; and
Department of Pediatrics, National Cheng Kung University, Tainan, Taiwan
Upon encountering the relevant vascular bed, lymphocytes attach to
endothelial adhesion molecules, transmigrate out of circulation, and
localize within tissues. Lymphocytes may then be retained at
microanatomic sites, as in tissues, or they may continue to migrate to
the lymphatics and recirculate in the blood. Lymphocytes also interact
transiently, but with high avidity, with target cells or APC that are
infected with microbes or have taken up exogenous foreign Ags. This
array of adhesive capabilities is mediated by the selective expression
of lymphocyte adhesion molecules. Here, we developed the 6F10 mAb,
which recognizes a cell surface glycoprotein designated lymphocyte
endothelial-epithelial cell adhesion molecule (LEEP-CAM), that is
distinct in biochemical characteristics and distribution of expression
from other molecules known to play a role in lymphocyte adhesion.
LEEP-CAM is expressed on particular epithelia, including the suprabasal
region of the epidermis, the basal layer of bronchial and breast
epithelia, and throughout the tonsillar and vaginal epithelia. Yet, it
is absent from intestinal and renal epithelia. Interestingly, it is
expressed also on vascular endothelium, especially high endothelial
venules (HEV) in lymphoid organs, such as tonsil and appendix. The
anti-LEEP-CAM mAb specifically blocked T and B lymphocyte adhesion
to monolayers of epithelial cells and to vascular endothelial cells in
static cell-to-cell binding assays by 
40–60% when compared with
control mAbs. These data suggest a role for this newly identified
molecule in lymphocyte binding to endothelium, as well as adhesive
interactions within selected epithelia.
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