LFA‐3 (CD58) Mediates T‐Lymphocyte Adhesion in Chronic Inflammatory Infiltrates

Abstract

Previous studies have suggested that LFA-3 has an important role in a number of chronic inflammatory pathologies, although an active role for LFA-3 within in vivo inflammatory reactions has not previously been directly observed in humans. To assess the importance of LFA-3 in this process, this study used an adaptation of the Stamper-Woodruff lymphocyte adhesion assay to measure the binding of exogenous activated lymphocytes to the T-cell-dominated chronic inflammatory infiltrate of oral lichen planus. Antibody blockade experiments showed that anti-LFA-3 monoclonal antibody reduced lymphocyte adhesion by approximately 29%, while anti-ICAM-1 produced a reduction of 26%. These results thus suggest that both LFA-3 and ICAM-1 are likely to mediate cell-cell interactions within lesional tissues in vivo. Moreover, these findings are also the first to directly demonstrate that LFA-3-mediated adhesion, like that of ICAM-1, is functionally important in the molecular pathology of inflammatory mucosal disease.

Soluble and Cell-Associated Forms of the Adhesion Molecule LFA-3 (CD58) are Differentially Regulated by Inflammatory Cytokines

“…We have shown previously that tissue expression of LFA-3 is upregulated under certain conditions in vivo (Kirby et al, 1995a), and recently we have reported that this is reflected in elevated binding of CD2-expressing T lymphocytes to the tissue in vitro (Kirby et al, 1999). In addition, in preliminary experiments not shown here, we have also found that the relative level of T cell adhesion to several different types of cell, as used in the present study, is proportional to the level of LFA-3 expressed by those cells.…”