Pathogenesis of rheumatoid arthritis

Thomas, Ranjeny and Cope, Andrew P. (2013). Pathogenesis of rheumatoid arthritis. In Richard A. Watts, Philip G. Conaghan, Christopher Denton, Helen Foster, John Isaacs and Ulf Müller-Ladner (Ed.), Oxford Textbook of Rheumatology 4th ed. (pp. 839-848) Oxford, United Kingdom: Oxford University Press. doi:10.1093/med/9780199642489.001.0001

Author Thomas, Ranjeny
Cope, Andrew P.
Title of chapter Pathogenesis of rheumatoid arthritis
Title of book Oxford Textbook of Rheumatology
Place of Publication Oxford, United Kingdom
Publisher Oxford University Press
Publication Year 2013
Sub-type Chapter in textbook
DOI 10.1093/med/9780199642489.001.0001
Edition 4th
ISBN 9780199642489
Editor Richard A. Watts
Philip G. Conaghan
Christopher Denton
Helen Foster
John Isaacs
Ulf Müller-Ladner
Chapter number 109
Start page 839
End page 848
Total pages 10
Total chapters 173
Language eng
Formatted Abstract/Summary
In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.
Q-Index Code BX
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Book Chapter
Collection: UQ Diamantina Institute - Open Access Collection
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Created: Thu, 20 Mar 2014, 21:11:39 EST by Kylie Hengst on behalf of UQ Diamantina Institute