The human intercellular adhesion molecules ICAM-1, ICAM-2 and their counter-receptors, the beta 2 or leukointegrins, mediate a variety of homotypic and heterotypic leukocyte and endothelial cell-cell adhesions central to immunocompetence. It has been found that cell-cell adhesion which is dependent on expression of the leukocyte function-associated antigen LFA-1 is not always blocked completely by antibodies raised against ICAM-1 and ICAM-2. Other leukointegrin ligands therefore probably exist, such as a glycoprotein of M(r) 124K that binds LFA-1 and has been designated ICAM-3 on the basis of this function. We have molecularly cloned a new member of the ICAM family, ICAM-R, which is related to ICAM-1 and ICAM-2. The complementary DNA encoding ICAM-R is 1,781 base pairs long and the protein has five extracellular immunoglobulin-family type domains. The mature cell-surface form of the ICAM-R protein has an M(r) which varies from 116 to 140K in a cell type-specific fashion. Overall identities in protein sequence with ICAM-1 and ICAM-2 are 48% and 31% respectively, with the degree of similarity varying between individual domains. The high level of expression of ICAM-R on resting leukocytes of all lineages and its lack of expression on either resting or cytokine-activated endothelial cells indicates a pattern of expression distinct from ICAM-1 and ICAM-2. In common with ICAM-1 and ICAM-2, ICAM-R is a ligand for the beta 2-integrin CD11a/LFA-1 (CD18).

Rationale: Chorioamnionitis is paradoxically associated with a decreased incidence of respiratory distress syndrome in preterm infants. In preterm lambs, intraamniotic endotoxin and interleukin 1 (IL-1) induce lung inflammation followed by lung maturation. Keywords: bronchopulmonary dysplasia; CD18; chorioamnionitis; respiratory distress syndrome; surfactant Chorioamnionitis or infection/inflammation of the fetal membranes and amniotic fluid is a pregnancy complication associated with up to 70% of all preterm deliveries at less than 30-wk

Anti-CD14 monoclonal antibody has the capacity to interfere with the innate immune response and systemic microbial clearance in experimental animals with E. coli bacteremia. The concomitant administration of effective antimicrobial therapy eliminated differences in the rate of microbial clearance between the control antibody and the CD14 monoclonal antibody. These results indicate that care should be taken in clinical trials with anti-CD14 monoclonal antibodies to ensure that adequate antimicrobial therapy is administered in the presence of systemic bacterial infection.