Abstract:
Cell adhesion molecules (CAM) including the intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) are from the immunoglobulin family which regulates leukocyte adherence to endothelial muscles in acute or chronic inflammatory states [1]. TNF-α, a proinflammatory cytokine, triggers cell adhesion molecules, inflammatory molecules, and other cytokines [2]. The appearance level of these CAMs on the membrane of endothelial cells is a key factor in determining the comparable impact of VCAM-1 and ICAM-1 on the attraction of leukocytes in a particular disease state [1,2]. Leukocytes and endothelial cells are two cell types that express ICAM-1 an Ig-like cell adhesion molecule. Transcriptional regulation is primarily responsible for regulating ICAM-1 expression. The ICAM-1 is critically important in inflammation and the T-cell-mediated immune response. Antigen-presenting cells use it to stimulate T cells that recognize only MHC class II antigens, whereas other cells use it to stimulate cytotoxic T cells by associating with MHC class I. Leukocyte migration to the inflammatory site is done by ICAM-1 [3]. It has a significant role in inflammation-related processes and the defense system mediated by T-cells [1]. VCAM-1 is the other inflammatory cell adhesion molecule that may be therapeutically useful in immunological disorders and cancerous conditions. VCAM-1 controls the inflammatory vascular adhesion and leukocyte trans-endothelial migration [2].
