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LFA‐3 (CD58) Mediates T‐Lymphocyte Adhesion in Chronic Inflammatory Infiltrates
Author(s) -
Alun C. Kirby,
Cahen,
Stephen Porter,
; Olsen
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00615.x
Subject(s) - lymphocyte function associated antigen 1 , lymphocyte , immunology , monoclonal antibody , in vivo , inflammation , adhesion , cell adhesion molecule , t lymphocyte , antibody , cell adhesion , icam 1 , biology , pathology , medicine , chemistry , immune system , microbiology and biotechnology , organic chemistry
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 ≈ 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.