Author(s): Hsu HC, Wu Y, Mountz JD
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Abstract The current studies of apoptosis in rheumatoid arthritis (RA) suggest that the TNF ligand-receptor superfamily (TNFRsF) molecules, downstream pathways (activation of proapoptosis or anti-apoptosis pathway), cell types (lymphocytes and synovial fibroblast), and the mechanism that triggers apoptosis (tolerance induction-related, downmodulation of inflammation-related, or DNA damage-related) all exhibit a capability to determine the induction or prevention of RA. This series of defects at different levels and in different cells have been shown to lead to T cell and synovial hyperproliferation, defective apoptosis, excessive apoptosis, or bone erosion. In this chapter, we summarize the available knowledge of the regulation of TNFRsF and their likely pathogenic roles in RA to help identify candidate target cells and target molecules for delivery of gene constructs to modulate apoptosis to prevent the development of RA in both humans and mice.
This article was published in Curr Dir Autoimmun
and referenced in Journal of Clinical & Cellular Immunology