Volume 233, Issue 1 pp. 256-266

Fibroblast-like synoviocytes in inflammatory arthritis pathology: the emerging role of cadherin-11

Sook Kyung Chang

Sook Kyung Chang

Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Havard Medical School, Boston, MA, USA.

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Zhizhan Gu

Zhizhan Gu

Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Havard Medical School, Boston, MA, USA.

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Michael B. Brenner

Michael B. Brenner

Division of Rheumatology, Immunology and Allergy, Brigham and Women’s Hospital, Havard Medical School, Boston, MA, USA.

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First published: 23 December 2009
Citations: 122
Michael B. Brenner
Theodore B. Bayles Professor of Medicine, Harvard Medical School
Chief, Division of Rheumatology, Immunology and Allergy Brigham and Women’s Hospital, Boston
Smith Building, Room 552
One Jimmy Fund Way
Boston, MA 02115, USA.
Tel.: +1 617 525 1000
Fax: +1 617 525 1001
e-mail: [email protected]

Abstract

Summary: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease affecting the joint synovium. The normal synovium consists of a lining layer of fibroblast-like synoviocytes (FLS) and macrophages, one to three cells deep that overlies the loose connective tissue of the synovial sublining. During the course of RA, the synovium is the site of inflammation where immune cells are massively infiltrated, and the lining layer becomes hyperplastic and transforms into a pannus tissue that destroys articular cartilage and bone. FLS play an important role in this RA pathogenesis. In this review, we explain that cadherin-11, an adhesion molecule, is selectively expressed on FLS and required for synovial lining formation. In addition, cadherin-11 on FLS contributes to synovial inflammation and mediates cartilage degradation in a mouse model of inflammatory arthritis. Therefore, we suggest that FLS are critical regulators of synovial inflammation and arthritis pathology via mechanisms that are mediated by cadherin-11.

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