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

Palmer-Lourenco, Gaby; Busso, Nathalie; Aurrand-Lions, Michel; Talabot Frischknecht-Ayer, Dominique; Chobaz-Peclat, Veronique; Zimmerli, Claudia; Hammel, Philippe; Imhof, Beat; Gabay, Cem

doi:10.1186/ar2223

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Title		Expression and function of junctional adhesion molecule-C in human and experimental arthritis
Authors		Palmer-Lourenco, Gaby Busso, Nathalie Aurrand-Lions, Michel Talabot Frischknecht-Ayer, Dominique Chobaz-Peclat, Veronique Zimmerli, Claudia Hammel, Philippe Imhof, Beat Gabay, Cem show all authors [1 - 9]
Published in		Arthritis Research and Therapy. 2007, vol. 9, no. 4, p. R65
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.
Keywords		Adoptive Transfer — Animals — Antibodies, Blocking/pharmacology — Arthritis, Experimental/drug therapy/ metabolism/pathology — Arthritis, Rheumatoid/ metabolism/pathology — Cell Adhesion Molecules/genetics/immunology/ metabolism — Cells, Cultured — Disease Models, Animal — Fibroblasts/drug effects/metabolism/pathology — Gene Expression — Humans — Immunoglobulins/genetics/immunology/ metabolism — Macrophages — Male — Membrane Proteins/genetics/immunology/ metabolism — Mice — Mice, Inbred C57BL — Mice, Transgenic — Neutrophils — Osteoarthritis/ metabolism/pathology — RNA, Messenger/metabolism — Serum Amyloid A Protein/analysis — Spleen/drug effects/pathology — Synovial Membrane/chemistry/ metabolism — T-Lymphocytes/drug effects/pathology
Identifiers		DOI: 10.1186/ar2223 PMID: 17612407
Full text		Article - Free access Other version: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2206366/pdf/ar2223.pdf
Structures		Faculté de médecine / Section de médecine clinique / Département de médecine
Research group		Mécanisme de l'inflammation articulaire (44)
Citation (ISO format)		PALMER-LOURENCO, Gaby et al. Expression and function of junctional adhesion molecule-C in human and experimental arthritis. In: Arthritis Research and Therapy, 2007, vol. 9, n° 4, p. R65. doi: 10.1186/ar2223 https://archive-ouverte.unige.ch/unige:11002