ICAM-1 (CD54) is a counter-receptor for Mac-1 (CD11b/CD18), as demonstrated through multiple binding assays and cell experiments. The study shows that purified Mac-1 binds to ICAM-1, and vice versa, indicating a direct interaction between these molecules. This interaction is crucial for the adhesion of stimulated neutrophils to endothelial cells, a key step in the immune response to infection. The study also reveals that ICAM-1 is involved in the adhesion of neutrophils to endothelial cells through both LFA-1 and Mac-1, suggesting that ICAM-1 serves as a common receptor for these integrins. However, the study also highlights that Mac-1 may interact with additional ligands on endothelial cells, as evidenced by the partial inhibition of adhesion by ICAM-1 mAbs. The findings support the role of ICAM-1 in mediating adhesion between neutrophils and endothelial cells, and they provide evidence that Mac-1 is a counter-receptor for ICAM-1. The study also discusses the importance of the CD11/CD18 family of integrins in immune functions, and the clinical relevance of leukocyte adhesion deficiency, a syndrome characterized by a deficiency in the common β chain of these integrins. The study concludes that ICAM-1 is a counter-receptor for Mac-1 and that this receptor pair is responsible for the adhesion between stimulated neutrophils and endothelial cells.ICAM-1 (CD54) is a counter-receptor for Mac-1 (CD11b/CD18), as demonstrated through multiple binding assays and cell experiments. The study shows that purified Mac-1 binds to ICAM-1, and vice versa, indicating a direct interaction between these molecules. This interaction is crucial for the adhesion of stimulated neutrophils to endothelial cells, a key step in the immune response to infection. The study also reveals that ICAM-1 is involved in the adhesion of neutrophils to endothelial cells through both LFA-1 and Mac-1, suggesting that ICAM-1 serves as a common receptor for these integrins. However, the study also highlights that Mac-1 may interact with additional ligands on endothelial cells, as evidenced by the partial inhibition of adhesion by ICAM-1 mAbs. The findings support the role of ICAM-1 in mediating adhesion between neutrophils and endothelial cells, and they provide evidence that Mac-1 is a counter-receptor for ICAM-1. The study also discusses the importance of the CD11/CD18 family of integrins in immune functions, and the clinical relevance of leukocyte adhesion deficiency, a syndrome characterized by a deficiency in the common β chain of these integrins. The study concludes that ICAM-1 is a counter-receptor for Mac-1 and that this receptor pair is responsible for the adhesion between stimulated neutrophils and endothelial cells.