LFA-3 (CD58) mediates T-lymphocyte adhesion in chronic inflammatory infiltrates.
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.
Kirby
A C
AC
Department of Oral Medicine, Eastman Dental Institute for Oral Health Care Sciences, University College London, University of London, UK.
Cahen
P
P
Porter
S R
SR
Olsen
I
I
D000328:Adult; D000911:Antibodies, Monoclonal; D018968:CD58 Antigens / Q000378:metabolism*; D016022:Case-Control Studies; D002448:Cell Adhesion / Q000276:immunology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D017676:Lichen Planus, Oral / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology
D000911:Antibodies, Monoclonal; D018968:CD58 Antigens