The chapter discusses the role of cell adhesion molecules (CAMs) and chemoattractant/activator molecules in the adhesion cascade that mediates neutrophil recruitment to sites of inflammation. The initial phase, characterized by the transient slowing of neutrophils in postcapillary venules, is driven by selectins. Subsequently, firm adhesion occurs through the interaction of CD11/CD18 integrins with endothelial ligands like ICAM-1, facilitated by activation by chemoattractants such as platelet-activating factor or interleukin-8. Transmigration into tissues requires both chemotactic stimuli and engagement of PECAM-1. Various approaches, including blocking antibodies, chimeric proteins, and genetically modified animals, have been used to study the role of CAMs in vivo, demonstrating that CAM blockade can effectively inhibit inflammation. The chapter highlights the importance of understanding the specific CAM/chemoattractant profiles in different inflammatory diseases to develop targeted therapies.The chapter discusses the role of cell adhesion molecules (CAMs) and chemoattractant/activator molecules in the adhesion cascade that mediates neutrophil recruitment to sites of inflammation. The initial phase, characterized by the transient slowing of neutrophils in postcapillary venules, is driven by selectins. Subsequently, firm adhesion occurs through the interaction of CD11/CD18 integrins with endothelial ligands like ICAM-1, facilitated by activation by chemoattractants such as platelet-activating factor or interleukin-8. Transmigration into tissues requires both chemotactic stimuli and engagement of PECAM-1. Various approaches, including blocking antibodies, chimeric proteins, and genetically modified animals, have been used to study the role of CAMs in vivo, demonstrating that CAM blockade can effectively inhibit inflammation. The chapter highlights the importance of understanding the specific CAM/chemoattractant profiles in different inflammatory diseases to develop targeted therapies.