Lymphocyte Adhesion to Epithelia and Endothelia Mediated by the Lymphocyte Endothelial-Epithelial Cell Adhesion Molecule Glycoprotein
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 i...
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description | 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 approximately 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. |
doi_str_mv | 10.4049/jimmunol.163.3.1592 |
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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 approximately 40-60% when compared with control mAbs. 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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 approximately 40-60% when compared with control mAbs. 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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 approximately 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.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>10415064</pmid><doi>10.4049/jimmunol.163.3.1592</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies, Blocking - chemistry Antibodies, Blocking - metabolism Antibodies, Blocking - physiology Antibodies, Monoclonal - chemistry Antibodies, Monoclonal - metabolism Antibodies, Monoclonal - physiology Binding Sites, Antibody Binding, Competitive - immunology Cations, Divalent - chemistry Cell Adhesion - immunology Cell Adhesion Molecules - chemistry Cell Adhesion Molecules - immunology Cell Adhesion Molecules - physiology Cell Line Endothelium, Vascular - chemistry Endothelium, Vascular - immunology Endothelium, Vascular - physiology Epithelial Cells - immunology Glycoside Hydrolases - metabolism Humans Intestinal Mucosa Leukocytes - metabolism Lymphocytes - immunology Lymphocytes - physiology Membrane Glycoproteins - chemistry Membrane Glycoproteins - immunology Membrane Glycoproteins - physiology Organ Specificity - immunology Precipitin Tests Staining and Labeling |
title | Lymphocyte Adhesion to Epithelia and Endothelia Mediated by the Lymphocyte Endothelial-Epithelial Cell Adhesion Molecule Glycoprotein |
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