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Apoptosis and rheumatoid arthritis: Past, present, and future directions

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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 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.

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Authors and Affiliations

  1. Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, 701 South 19th Street, LHRB 473, 35294-0007, Birmingham, AL, USA

    John D. Mountz MS, PhD

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  1. John D. Mountz MS, PhD
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  2. Hui-Chen Hsu PhD
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  3. Yasunori Matsuki MD
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  4. Huang-Ge Zhang PhD, DVM
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Mountz, J.D., Hsu, HC., Matsuki, Y. et al. Apoptosis and rheumatoid arthritis: Past, present, and future directions. Curr Rheumatol Rep 3, 70–78 (2001). https://doi.org/10.1007/s11926-001-0053-y

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  • DOI: https://doi.org/10.1007/s11926-001-0053-y

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