Search

Homotypic adhesion by phorbol ester-stimulated lymphocytes requires LPA-1 and MC2 and does not involve like-like interactions between LFA-1 molecules on adjacent cells. The latter finding suggested that a second molecule, distinct from LFA-1, also participates in LFA-1-dependent adhesion. The identification of such a molecule was the object of this investigation. After immunization with LFA-1 deficient EBV-transformed lymphoblastoid cells, a MAb was obtained that inhibits phorbol ester-stimulated aggregation of LFA-P EBV lines. This MAb defines a novel cell surface molecule, which is designated intercellular adhesion molecule 1 (ICAM1). ICAM-l is distinct from LFA-1 in both cell distribution and structure. In SDS-PAGE, ICAM-l isolated from JY cells is a single chain of M. = 90,000. As shown by MAb inhibition, ICAM-l participates in phorbol ester-stimulated adhesion reactions of B lymphocyte and myeloid cell lines and T lymphocyte blasts. However, aggregation of one T lymphocyte cell line (SKW-3) was inhibited by LFA-1 but not ICAM-1 MAb. It is proposed that ICAM-l may be a ligand in many, but not all, LFA-l-dependent adhesion reactions. [ABSTRACT FROM AUTHOR]