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MR Vol.12 No.2 indexに戻る
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MODERN RHEUMATOLOGY
Vol.12 No.2 |
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Chemokines in synovial inflammation in
rheumatoid arthritis: basic and clinical aspects |
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| K. Tani1, T. Shimizu1, Y. Motoki1, S. Sone1 |
| (1)Third Department of Internal Medicine, School
of Medicine, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima
770-8503, Japan |
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| Abstract |
| Abstract Rheumatoid arthritis (RA) is a chronic,
multisystem autoimmune disease characterized by persistent synovitis.
Since chemotactic cytokines (chemokines) may play critical roles
in the recruitment of leukocytes in RA, analyses of chemokines
and their receptors should provide insight into events in synovial
inflammation in RA. The production of chemokines is regulated by
cytokines such as tumor necrosis factor (TNF)-! produced in the
inflamed joint, suggesting that the efficacy of anti-TNF-! therapy
is mediated at least partly by the reduction of chemokine production.
Chemokines have a role in joint inflammation not only by inducing
leukocyte chemotaxis, but also by activating immune cells and angiogenesis.
The pathogenesis of RA has been shown to be mediated by Th1-type
T cells, because Th1-related chemokine receptors are preferentially
expressed on cells in synovial fluid and synovial tissue. Accordingly,
antichemokine therapy may be important as a possible new approach
to therapeutic intervention in RA. |
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| Key words |
| Key words Angiogenesis ・ Chemokine ・ Chemotaxis
・ Rheumatoid arthritis (RA) ・ Th-1 |
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