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.

• Authors: A C Kirby, P Cahen, S R Porter, I Olsen
• Journal: Scandinavian journal of immunology (Scand J Immunol) Vol. 50 Issue 5 Pg. 469-74 (Nov 1999) ISSN: 0300-9475 [Print] England
• PMID: 10564548 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Monoclonal
• CD58 Antigens

Topics

• Adult
• Antibodies, Monoclonal
• CD58 Antigens (metabolism)
• Case-Control Studies
• Cell Adhesion (immunology)
• Female
• Humans
• In Vitro Techniques
• Inflammation (immunology, pathology)
• Lichen Planus, Oral (immunology, pathology)
• Lymphocyte Activation
• Male
• Middle Aged
• T-Lymphocytes (immunology, pathology)