Expression of adhesion molecules in synovia of patients with treatment-resistant Lyme arthritis

Citation
E. Akin et al., Expression of adhesion molecules in synovia of patients with treatment-resistant Lyme arthritis, INFEC IMMUN, 69(3), 2001, pp. 1774-1780
Citations number
36
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
69
Issue
3
Year of publication
2001
Pages
1774 - 1780
Database
ISI
SICI code
0019-9567(200103)69:3<1774:EOAMIS>2.0.ZU;2-J
Abstract
The expression of adhesion molecules in synovium in patients with Lyme arth ritis is surely critical in the control of Borrelia burgdorferi infection b ut may also have pathologic consequences. For example, molecular mimicry be tween a dominant T-cell epitope of B, burgdorferi outer surface protein A a nd an adhesion molecule, human lymphocyte function-associated antigen 1 (LF A-1), has been implicated in the pathogenesis of treatment-resistant Lyme a rthritis. Using immunohistochemical methods, we examined synovial samples f or expression of adhesion molecules in 29 patients with treatment-resistant Lyme arthritis and in 15 patients with rheumatoid arthritis or chronic inf lammatory monoarthritis, In Lyme arthritis synovia, endothelial cells showe d intense expression of P-selectin and vascular adhesion protein-1 (VAP-1), Expression of LFA-1 was also intense on infiltrating cells, particularly i n lymphoid aggregates, and intercellular adhesion molecule-1 (ICAM-1) was m arkedly expressed on synovial lining and endothelial and infiltrating cells , Moderate expression of vascular cell adhesion molecule-1 (VCAM-1) was see n on synovial lining and endothelial cells, and mild expression of its liga nd, very late antigen-4, was apparent in perivascular lymphoid infiltrates. Except for lesser expression of VCAM-1 in Lyme synovia, the levels of expr ession of these adhesion molecules were similar in the three patient groups , We conclude that certain adhesion molecules, including ICAM-1 and LFA-1, are expressed intensely in the synovia of patients with Lyme arthritis. Upr egulation of LFA-1 on lymphocytes in this lesion may be critical in the pat hogenesis of treatment-resistant Lyme arthritis.