Mechanisms of Disease: the molecular and cellular basis of joint destruction in rheumatoid arthritis
Author:
Publisher
Springer Science and Business Media LLC
Subject
Rheumatology
Link
http://www.nature.com/articles/ncprheum0047.pdf
Reference50 articles.
1. Neumann E et al. (2002) Identification of differentially expressed genes in rheumatoid arthritis by a combination of complementary DNA array and RNA arbitrarily primed-polymerase chain reaction. Arthritis Rheum 46: 52–63
2. Faour WH et al. (2005) Early growth response factor-1 mediates prostaglandin E2-dependent transcriptional suppression of cytokine-induced tumor necrosis factor-α gene expression in human macrophages and rheumatoid arthritis-affected synovial fibroblasts. J Biol Chem 280: 9536–9546
3. Garcia-Vicuna R et al. (2004) CC and CXC chemokine receptors mediate migration, proliferation, and matrix metalloproteinase production by fibroblast-like synoviocytes from rheumatoid arthritis patients. Arthritis Rheum 50: 3866–3877
4. Kasperkovitz PV et al. (2005) Fibroblast-like synoviocytes derived from patients with rheumatoid arthritis show the imprint of synovial tissue heterogeneity: evidence of a link between an increased myofibroblast-like phenotype and high-inflammation synovitis. Arthritis Rheum 52: 430–441
5. Firestein GS (2003) Evolving concepts of rheumatoid arthritis. Nature 423: 356–361
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