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Role of TNF-¦Á in Rheumatoid Arthritis (pp. 29-52) $100.00
Authors:  (Guangjie Chen, Jian Hong, Department of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai Institute of Immunology, Shanghai, China, and others)
Rheumatoid arthritis (RA) is characterized by chronic inflammation
of the synovium of peripheral joints. Although the etiology and
pathogenesis of RA are still not fully understood, it is generally
considered an autoimmune disease in which proinflammatory cytokines
known to be produced primarily by macrophages and connective tissue
cells (fibroblasts) are expressed in abundance in RA synovium and
synovial fluid. These cytokines, including tumor necrosis factor (TNF),
IL-1, IL-6, IL-8, and granulocyte–macrophage colony-stimulating factor
(GM-CSF), regulate a broad range of inflammatory processes in the
pathogenesis of RA. In particular, TNF- is found in large quantities in
the rheumatoid joint. It has been recognized as a key pathogenic cytokine
that drives a pathogenic cytokine milieu leading to tissue damage. TNFpromotes
osteoclast differentiation and activates osteoclasts, leading to joint erosions. The regulation of different immune cells by TNF- is
another major cause of the dysregulation of immune homeostasis in RA.
TNF- antagonists were the first of the biological DMARDs approved
for the treatment of RA. Anti-TNF- antibody treatments significantly
reduce the production of other pro-inflammatory cytokines, including IL-
1 and IL-6 and the release of chemokines that attract leukocytes from the
blood into the inflamed tissue. In this chapter, we review the regulation of
inflammation by TNF- in connection with different cell types in the
pathogenesis of rheumatoid arthritis. 

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Role of TNF-¦Á in Rheumatoid Arthritis (pp. 29-52)