PATHOLOGY

Detailed explanation-1: -Intercellular adhesion molecule 1 (ICAM-1, CD54) binds to the integrin LFA-1 (CD11a/CD18), promoting cell adhesion in immune and inflammatory reactions. ICAM-1 is also subverted as a receptor by the major group of rhinoviruses.

Detailed explanation-2: -Besides binding to LFA-1, the ICAM-1 peptide can be internalized by LFA-1 receptors into the cytoplasmic domain of T-cells. Therefore, this ICAM-1 peptide can be utilized to selectively target toxic drugs to T-cells, thus avoiding harmful side effects.

Detailed explanation-3: -The LFA-1/ICAM-1 interaction plays a role in the firm adhesion of T cells to the endothelium, followed by transmigration of T cells across endothelial cells via intracellular signals that lead to cytoskeletal changes necessary for cell movement.

Detailed explanation-4: -LFA-1 binds to three ligands that we have encountered before in our discussions of adhesion: ICAM-1 (CD54), ICAM-2 (CD102), and ICAM-3 (CD50) (Fig. 14-2). ICAM-1, a widely expressed membrane glycoprotein of 80–114 kDa, contains five extracellular Ig-like domains, making it another member of the Ig superfamily.

Detailed explanation-5: -Vascular endothelium expresses low levels of ICAM-1, and inflammatory stimuli can markedly increase ICAM-1 surface expression. In acute and chronic inflammatory diseases, endothelial cells become activated and express high levels of ICAM-1, in addition to vascular cell adhesion molecule-1 (VCAM-1) and E-selectin.