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Common Mechanisms in Immune-Mediated Inflammatory Disease
GARY S. FIRESTEIN and MARIPAT CORR
ABSTRACT.
Characterization of the K/BxN mouse model of spontaneous arthritis contributed to the rediscovery of immune complex-mediated inflammation in rheumatoid arthritis (RA). Serum from these animals can transfer joint-specific inflammation to normal mice. Fc receptors, interleukin 1, mast cells, and complement are all essential for the development of arthritis after serum transfer. In RA, additional amplifying factors have been identified, including cytokines and intracellular signaling molecules, such as mitogen-activated protein kinases and nuclear factor kappa B, that perpetuate inflammation. Understanding the autoimmune and inflammatory pathways implicated in disease has led to targeted drug development and improved clinical outcomes. (J Rheumatol 2005;32 Suppl 73:8-13)
Key Indexing Terms:
RHEUMATOID ARTHRITIS
PATHOGENESIS
DISEASE MODELS, ANIMAL
TOLL-LIKE RECEPTORS
CYTOKINES
NUCLEAR FACTOR KAPPA B
From the Division of Rheumatology, Allergy, and Immunology, Department of Medicine, University of California at San Diego, San Diego, California, USA.
This educational activity is sponsored by the University of Texas Southwestern Medical Center at Dallas, which is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians, through an unrestricted educational grant from Genentech, Inc. and Biogen Idec Inc.
G.S. Firestein, MD, Professor of Medicine; M. Corr, MD, Associate Professor of Medicine.
Address reprint requests to Dr. G.S. Firestein, Division of Rheumatology, Allergy, and Immunology, Department of Medicine, University of California at San Diego, La Jolla, California, USA.
E-mail: gfirestein@ucsd.edu
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