ABSTRACT
Autoimmune rheumatic diseases result from a process involving three distinct but related components – a break in self-tolerance, development of chronic inflammation in one or several organs, and if ongoing, tissue destruction and its resultant detrimental effects. It has been proposed that dendritic cells (DCs) are the critical decision-making cells in the immune system.1
Through their role in the generation of central and peripheral tolerance, as well as in priming immune responses and stimulation of memory and effector T cells, DCs are likely to play essential roles in both the initiation and perpetuation of autoimmunity and autoimmune diseases. However, the understanding of the means by which DCs contribute to peripheral tolerance has opened the exciting possibility of harnessing them for antigen-specific immunotherapy of autoimmune diseases and transplantation. This chapter will consider the use of DCs as a biological therapy for the induction of tolerance in rheumatic autoimmune diseases. After consideration of the known mechanisms of peripheral tolerance, we will focus on the various means by which effector function is regulated in the periphery. Means and pathways by which DCs have induced peripheral tolerance in autoimmune models will be discussed, followed by consideration of the potential and relative merits of
