The immune system maintains the integrity of our bodies by warding off intruding microorganisms, but by sustaining tolerance to our own tissues. The immunologic tolerance is established by several layers of safeguards, including physical elimination of self-reactive lymphocytes during their development in the central lymphoid organs, anergy induction in autoreactive lymphocytes before their emigration to the periphery, or production regulatory T lymphocytes that suppress the activation, proliferation, and differentiation of various effector cells. The major regulatory T lymphocytes display their phenotype as CD4(+)CD25(+)Foxp3(+) and constitute about 10% of the peripheral T lymphocytes. Even with these safeguards, the immunologic tolerance sometimes fails and generates autoimmune diseases. Scientists studying the pathogenesis of autoimmune diseases pay particular attention to a CD4(+) T lymphocytes subset, Th17 lymphocytes, distinct from Th1 and Th2. Th17 produces diverse proinflammatory cytokines including IL-17 and TNF-alpha. Th17 and these cytokines are causatively associated with many episodes of autoimmune diseases. Accumulated data reveal the critical role of Th17 cells in the pathology of autoimmunity and portray them as an important target in the treatment of various autoimmune diseases. In this article, we will describe the main characteristics of regulatory T cells and Th17 cells and their cellular and molecular mechanisms of protective or destructive functions, respectively.