Introduction

Although the cause of autoimmune diseases is largely obscure at present, it is well established that T cells are the key mediators of many autoimmune diseases as the effectors of cell-mediated immunity and helper T cells for autoantibody formation [1]. It has also been well demonstrated that T cells that are reactive with normal self-antigens and hence potentially pathogenic are present in normal individuals [2, 3]. Fundamental questions for understanding the cause and mechanism of autoimmune disease are, therefore, what specificities and potencies of self-reactive T cells can be produced by the thymus, how their activation and expansion is physiologically controlled in the periphery, and what conditions are required for their activation and expansion to cause autoimmune disease. In addition, given that both genetic and environmental factors contribute to the pathogenetic process ofcommon autoimmune diseases, such as type 1 diabetes (T1D) and rheumatoid arthritis, one can ask how genetic and environmental factors affect the control of thymic production and peripheral activation/expansion of self-reactive T cells.

There is accumulating evidence that, in addition to clonal deletion or inac-tivation of self-reactive T cells, T cell-mediated dominant control is another important mechanism of immunologic self-tolerance (see [4-7] for review). The normal immune system harbors naturally arising regulatory T cells (Treg) that engage in suppressing the activation and expansion of pathogenic self-

reactive T cells in the periphery, thereby preventing autoimmune disease. Impaired thymic development of natural Treg or their abnormality in number or function in the periphery indeed leads to the spontaneous occurrence of various organ-specific autoimmune diseases in otherwise normal rodents and also in humans [7]. Based on recent findings, we shall discuss in this article a possible mechanism of autoimmune disease due to impaired immunoregulation mediated by natural Treg.

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