ABSTRACT
Autoimmune diseases can be roughly divided into organ-specific and systemic, based both on the extent of their involvement and the type of “autoantibodies” present in the patients. The systemic forms of autoimmune diseases, best-exemplified by systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), are discussed in Chapters 18 and 19. Less generalized autoimmune processes may affect virtually every organ system (Table 1); in many instances, only certain cell types within an organ system will be affected in a particular disease, that is, gastric parietal cells in pernicious anemia. In this chapter, we restrict our discussion to the major autoimmune diseases that affect specific organs and the associated autoantibodies, with the understanding that in many cases these antibodies are not the cause of the disease, but just a secondary manifestation. Our understanding of the pathogenesis of most organ-specific autoimmune disorders is schematically illustrated in Figure 1. The key cells are autoreactive T cells, which under the right circumstances become activated. The activated T cells can be controlled by T regulatory cells (Tregs), but if they manage to overcome the downregulating effects of those cells, then, both directly and through activated macrophages, they are able to cause the death of cells expressing the autoantigens that triggered the reaction.
