Expression and function of junctional adhesion molecule-C in human and experimental arthritis

Détails

Ressource 1Télécharger: BIB_BA2B4481251B.P001.pdf (2368.08 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_BA2B4481251B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Expression and function of junctional adhesion molecule-C in human and experimental arthritis
Périodique
Arthritis Research and Therapy
Auteur(s)
Palmer  G., Busso  N., Aurrand-Lions  M., Talabot-Ayer  D., Chobaz-Peclat  V., Zimmerli  C., Hammel  P., Imhof  B. A., Gabay  C.
ISSN
1478-6362 (Electronic)
Statut éditorial
Publié
Date de publication
07/2007
Volume
9
Numéro
4
Pages
R65
Notes
Journal article --- Old month value: Jul 5
Résumé
ABSTRACT: Junctional adhesion molecule-C (JAM-C) is an adhesion molecule involved in transendothelial migration of leukocytes. In this study, we examined JAM-C expression in the synovium and investigated the role of this molecule in two experimental mouse models of arthritis. JAM-C expression was investigated by reverse transcriptase-polymerase chain reaction and immunohistochemistry. The effects of a monoclonal anti-JAM-C antibody were assessed in antigen-induced arthritis (AIA) and K/BxN serum transfer-induced arthritis. JAM-C was expressed by synovial fibroblasts in the lining layer and associated with vessels in the sublining layer in human and mouse arthritic synovial tissue. In human tissue, JAM-C expression was increased in rheumatoid arthritis (RA) as compared to osteoarthritis synovial samples (12.7 +/- 1.3 arbitrary units in RA versus 3.3 +/- 1.1 in OA; p < 0.05). Treatment of mice with a monoclonal anti-JAM-C antibody decreased the severity of AIA. Neutrophil infiltration into inflamed joints was selectively reduced as compared to T-lymphocyte and macrophage infiltration (0.8 +/- 0.3 arbitrary units in anti-JAM-C-treated versus 2.3 +/- 0.6 in isotype-matched control antibody-treated mice; p < 0.05). Circulating levels of the acute-phase protein serum amyloid A as well as antigen-specific and concanavalin A-induced spleen T-cell responses were significantly decreased in anti-JAM-C antibody-treated mice. In the serum transfer-induced arthritis model, treatment with the anti-JAM-C antibody delayed the onset of arthritis. JAM-C is highly expressed by synovial fibroblasts in RA. Treatment of mice with an anti-JAM-C antibody significantly reduced the severity of AIA and delayed the onset of serum transfer-induced arthritis, suggesting a role for JAM-C in the pathogenesis of arthritis.
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 8:29
Dernière modification de la notice
20/08/2019 15:28
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