Redundant regulatory mechanisms in autoimmune diseases: The example of experimental autoimmune encephalomyelitis

In multiple sclerosis (MS) and in its animal model, Experimental Autoimmune Encephalomyelitis (EAE), autoagressive and regulatory cells traffic into the Central Nervous System (CNS), and may alter the course of the disease. Consequently the role of immunocompetent cells is major determinants in EAE pathogenesis for instance, CD4 T helper 1 cells, have been identified as a key element in determining the course of the disease; however other cells, can also induce EAE, and have pathogenic and regulatory roles in EAE pathogenesis (induction and recovery). Experimental autoimmune encephalomyelitis models are also useful tools in understanding the generation and organization of the myelin-specific autoimmune repertoires and immunoregulatory loops involved in spontaneous recovery. The aim of the present work is to outline how the pathogenic and the regulatory elements prevail in EAE, and correlate them with other autoimmune disorders. These effects of pathogenic and regulatory cells, need to be considered for efficacious therapy. A necessary step for the design of antigen-specific immunotherapies in the treatment of chronic autoimmune disorders in humans is to learn how manipulate the immune system, to know the biology of its cell populations.