Pathogenesis of rheumatoid arthritis: The role of synoviocytes

Citation
Y. Yamanishi et Gs. Firestein, Pathogenesis of rheumatoid arthritis: The role of synoviocytes, RHEUM DIS C, 27(2), 2001, pp. 355-371
Citations number
119
Categorie Soggetti
Rheumatology
Journal title
RHEUMATIC DISEASE CLINICS OF NORTH AMERICA
ISSN journal
0889857X → ACNP
Volume
27
Issue
2
Year of publication
2001
Pages
355 - 371
Database
ISI
SICI code
0889-857X(200105)27:2<355:PORATR>2.0.ZU;2-8
Abstract
Rheumatoid arthritis (RA) is traditionally considered to be a T-cell-mediat ed disease. Additional data have implicated T-cell-independent pathways in its pathogenesis, however, especially in late stages of the disease.(26, 32 ) No one can reasonably dispute that RA is a disease involving immunologic processes(34,84) ; however, the specific contribution of T cells as initiat ors or perpetuators of the disease remains difficult to prove. Non-T-cell e lements, including macrophage and fibroblast-like synoviocytes (FLS), are c apable of producing cytokines and matrix-degrading enzymes in the joint, pr oliferating, and invading adjacent tissues, perhaps in an autonomous fashio n. These non-T-cell participants could play an essential role in destructiv e aspects of the disease. In this article, we mainly focus on FLS among the se constituents of RA synovial tissues and discuss the characteristics of t hese cells in relation to transformation, signal transduction, and producti on of enzymes responsible for joint destruction.