Apoptosis and rheumatoid arthritis: Past, present, and future directions
- Cite this article as:
- Mountz, J.D., Hsu, HC., Matsuki, Y. et al. Curr Rheumatol Rep (2001) 3: 70. doi:10.1007/s11926-001-0053-y
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The current studies of apoptosis in rheumatoid arthritis (RA) suggest that molecules (Fas-related or TNF-related), pathways (activation of pro-apoptosis or anti-apoptosis pathway), cell types (lymphocytes or synovial fibroblast), and the mechanism that triggers apoptosis (tolerance induction-related, down-modulation of inflammationrelated, or DNA damage-related) all play a fundamental role to determine the induction or prevention of RA. These series of defects at different levels and in different cells lead to hyperproliferation, defective apoptosis, or hyperapoptosis. This review summarizes the available knowledge of apoptosis and RA to help identify candidate target cells and target molecules for delivery of gene constructs or modified biological or chemical reagents to the target site for effective modification of these cells.