LFA-3 (CD58) mediates T-lymphocyte adhesion in chronic inflammatory infiltrates

Citation
Ac. Kirby et al., LFA-3 (CD58) mediates T-lymphocyte adhesion in chronic inflammatory infiltrates, SC J IMMUN, 50(5), 1999, pp. 469-474
Citations number
30
Categorie Soggetti
Immunology
Journal title
SCANDINAVIAN JOURNAL OF IMMUNOLOGY
ISSN journal
03009475 → ACNP
Volume
50
Issue
5
Year of publication
1999
Pages
469 - 474
Database
ISI
SICI code
0300-9475(199911)50:5<469:L(MTAI>2.0.ZU;2-M
Abstract
Previous studies have suggested that LFA-3 has an important role in a numbe r of chronic inflammatory pathologies, although an active role for LFA-3 wi thin in vivo inflammatory reactions has not previously been directly observ ed 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 me asure the binding of exogenous activated lymphocytes to the T-cell-dominate d chronic inflammatory infiltrate of oral lichen planus. Antibody blockade experiments showed that anti-LFA-3 monoclonal antibody reduced lymphocyte a dhesion by approximate to 29%, while anti-ICAM-1 produced a reduction of 26 %. These results thus suggest that both LFA-3 and ICAM-1 are likely to medi ate cell-cell interactions within lesional tissues in vivo. Moreover, these findings are also the first to directly demonstrate that LFA-3-mediated ad hesion, like that of ICAM-1, is functionally important in the molecular pat hology of inflammatory mucosal disease.