The development of autoimmune diseases is characterized by the breakdown of mechanism(s) that are responsible for maintaining immunological tolerance against self-structures in the periphery. Several aberrations of immune cells have been described so far. Most recently quantitative and/or qualitative defects of T cells with the capacity to suppress or regulate the proliferation of effector T cells in vitro - subsequently termed regulatory T cells (Treg) - have been suggested to substantially contribute to the imbalance of peripheral tolerance and trigger the outbreak of autoimmune reactions. The aim of this article is to summarize current knowledge about pathomechanisms that are involved in the development of autoimmunity with a special emphasis on the role of Treg in patients with systemic lupus erythematosus (SLE).
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