INTERCELLULAR-ADHESION MOLECULE-1 DEFICIENCY PROLONGS SURVIVAL AND PROTECTS AGAINST THE DEVELOPMENT OF PULMONARY INFLAMMATION DURING MURINELUPUS

One of the characteristic features of the lupus syndrome in humans and mice is the organ-specific accumulation of leukocytes within a variet y of different tissues; however, the etiology of this phenomenon remai ns unclear. The work presented here determined the role of intercellul ar adhesion molecule (ICAM)-1 in the development of pulmonary leukocyt e accumulation by generating MRL/MpJ-Fas(1pr) mice that are geneticall y deficient in this critical adhesion molecule, Interestingly, these M RL/MpJ-Fas(1pr) ICAM-1 knockout mice exhibit prolonged survival times compared to littermates expressing ICAM-1. We have determined that lac k of ICAM-1 completely abrogates the development of pulmonary inflamma tion but does not prevent the development of autoantibodies, lymphaden opathy, and glomerulonephritis. Furthermore, the Lack of pulmonary inf lammation was found to be due to decreased migration of leukocytes to the lung rather than decreased in situ proliferation of cells.