PECAM-1 is essential for leukocyte transmigration through endothelial cell junctions. A monoclonal antibody against PECAM or recombinant soluble PECAM blocks transendothelial migration of monocytes by 70–90%. Pretreatment of monocytes or endothelial junctions with the antibody blocks migration. If the endothelium is activated by cytokines, the antibody or soluble PECAM still blocks migration of both monocytes and neutrophils. Anti-PECAM does not block chemotaxis. Light and electron microscopy show that leukocytes blocked in transmigration remain tightly bound to the apical surface of endothelial cells over the junctions. Leukocyte emigration involves three stages: rolling (selectins), tight adhesion (integrins), and transmigration (PECAM-1). Leukocytes leave the circulation by binding to the endothelium and migrating between endothelial cells. This process is constitutive in some cases, such as monocytes becoming tissue macrophages. Lymphocytes enter lymph nodes by binding to high endothelial venules. During inflammation, leukocytes migrate by binding to cytokine-induced adhesion molecules. PECAM-1, a member of the Ig superfamily, is concentrated in endothelial cell junctions and expressed on monocytes and neutrophils. It mediates adhesive interactions after integrin-mediated adhesion. Anti-PECAM blocks transmigration after tight adhesion. Leukocyte emigration is experimentally dissectable into three steps, each mediated by different adhesion molecules. PECAM-1 is crucial for transendothelial migration. Anti-PECAM antibodies block transmigration of monocytes and neutrophils. Soluble recombinant PECAM also blocks transmigration. Anti-PECAM does not affect chemotaxis. The effect is long-lasting but reversible. PECAM is concentrated in endothelial cell junctions and is accessible to antibodies. Anti-PECAM blocks transmigration of monocytes and neutrophils. PECAM plays a similar role in neutrophil transmigration as in monocytes. PECAM-1 is essential for transendothelial migration. Anti-PECAM reagents block transmigration of monocytes and neutrophils. PECAM-1 is involved in homophilic adhesion between leukocytes and endothelial cells. PECAM-1 may also activate β2 integrins through adhesion cascades. PECAM-1's role in transmigration is not mutually exclusive and is under investigation. PECAM-1 may have a role in the constitutive and inflammatory emigration of monocytes and neutrophils. PECAM-1 is expressed on various myeloid and lymphoid tumor cell lines. PECAM-1 may aid in the emigration of these cells during metastasis. PECAM-1 is essential for transendothelial migration. Anti-PECAM rePECAM-1 is essential for leukocyte transmigration through endothelial cell junctions. A monoclonal antibody against PECAM or recombinant soluble PECAM blocks transendothelial migration of monocytes by 70–90%. Pretreatment of monocytes or endothelial junctions with the antibody blocks migration. If the endothelium is activated by cytokines, the antibody or soluble PECAM still blocks migration of both monocytes and neutrophils. Anti-PECAM does not block chemotaxis. Light and electron microscopy show that leukocytes blocked in transmigration remain tightly bound to the apical surface of endothelial cells over the junctions. Leukocyte emigration involves three stages: rolling (selectins), tight adhesion (integrins), and transmigration (PECAM-1). Leukocytes leave the circulation by binding to the endothelium and migrating between endothelial cells. This process is constitutive in some cases, such as monocytes becoming tissue macrophages. Lymphocytes enter lymph nodes by binding to high endothelial venules. During inflammation, leukocytes migrate by binding to cytokine-induced adhesion molecules. PECAM-1, a member of the Ig superfamily, is concentrated in endothelial cell junctions and expressed on monocytes and neutrophils. It mediates adhesive interactions after integrin-mediated adhesion. Anti-PECAM blocks transmigration after tight adhesion. Leukocyte emigration is experimentally dissectable into three steps, each mediated by different adhesion molecules. PECAM-1 is crucial for transendothelial migration. Anti-PECAM antibodies block transmigration of monocytes and neutrophils. Soluble recombinant PECAM also blocks transmigration. Anti-PECAM does not affect chemotaxis. The effect is long-lasting but reversible. PECAM is concentrated in endothelial cell junctions and is accessible to antibodies. Anti-PECAM blocks transmigration of monocytes and neutrophils. PECAM plays a similar role in neutrophil transmigration as in monocytes. PECAM-1 is essential for transendothelial migration. Anti-PECAM reagents block transmigration of monocytes and neutrophils. PECAM-1 is involved in homophilic adhesion between leukocytes and endothelial cells. PECAM-1 may also activate β2 integrins through adhesion cascades. PECAM-1's role in transmigration is not mutually exclusive and is under investigation. PECAM-1 may have a role in the constitutive and inflammatory emigration of monocytes and neutrophils. PECAM-1 is expressed on various myeloid and lymphoid tumor cell lines. PECAM-1 may aid in the emigration of these cells during metastasis. PECAM-1 is essential for transendothelial migration. Anti-PECAM re