Autoimmunity is physiological: in every normal individual autoreactive T cells and B cells which produce natural autoantibodies, exist. Auto-immunity becomes pathological, giving rise to an autoimmune disease, when the number of autoreactive cells, and particularly the avidity of their receptors for autoantigens increase. Triggering of the disease depends both on the increase in immunogenicity of the target cell, which may be secondary to a viral infection, and the individual's own capability to recognize the antoantigens (HLA genes, T cell repertoire). More rarely, the disease is caused by an infectious agent leading to a crossed reaction with an autoantigen (Guillain-Barré syndrome). Nevertheless, all these elements are not sufficient to provoke a chronic disease such as multiple sclerosis or myasthenia gravis. The passage to chronicity is usually secondary to a defect in immunoregulation. Several categories of regulatory T cells have been found: Th2 cells, CD25+ cells, Trl cells, NKT cells. It is still difficult to asses the responsibility of the defect of one of these populations in a given disease, or to single out the cytokines implicated, although an essential role is often given to interleukin 10 and/or TGFB. Even if the pathogenic autoimmune reaction is triggered by the autoantigens of the target cell, there is apparently not a unique autoantigen target. The specificity of the reaction spreads progressively from one antigen, which may vary among subjects, to the entire target cell. It is based on these notions that new immunotherapeutic approaches for autoimmune diseases are being developed (soluble autoantigens, or one of their modified peptides: (APL), cytokine, anti-CD3 antibody).