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Apoptosis and rheumatoid arthritis: past, present, and future directions
J D Mountz1, H C Hsu, Y Matsuki
1Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, 701 South 19th Street, LHRB 473, Birmingham, AL 35294-0007, USA. John.Mountz@ccc.uab.edu
Abstract:
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 inflammation-related, 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.
Insights
Apoptosis defects in rheumatoid arthritis (RA) involve molecules, pathways, and cells, leading to abnormal cell proliferation or death. Understanding these mechanisms is key for developing targeted RA therapies.
Area of Science:
- Immunology
- Cell Biology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) pathogenesis involves complex dysregulation of programmed cell death (apoptosis).
- Key factors influencing RA include specific molecules (Fas, TNF), signaling pathways (pro-apoptosis, anti-apoptosis), and cell types (lymphocytes, synovial fibroblasts).
- Mechanisms triggering apoptosis defects in RA relate to tolerance induction, inflammation modulation, and DNA damage.
Purpose of the Study:
- To review current knowledge on apoptosis in rheumatoid arthritis.
- To identify potential cellular and molecular targets for therapeutic intervention in RA.
Main Methods:
- Literature review of studies on apoptosis and rheumatoid arthritis.
Main Results:
- Defects in apoptosis at various levels and in different cell types contribute to RA development.
- These defects can result in hyperproliferation, defective apoptosis, or hyperapoptosis in affected cells.
Conclusions:
- Targeting specific cells and molecules involved in apoptosis dysregulation offers a promising strategy for effective RA treatment.
- Further research can guide the delivery of gene constructs or biological/chemical reagents for RA therapy.