More specifically, the temporal pattern of the antigenic signal leads the immune system to develop either a large excess of Treg cells, in which case peripheral tolerance develops, or else a large excess of Th17 cells, in which case a defensive attack is mounted. We term this mechanism for immune system regulation the ��Growth Detection Paradigm��, or GDP, and suggest that it can rationalize many of the confusing aspects of T-cell interactions and immune system regulation. In particular, GDP offers a novel explanation for the development of peripheral tolerance, which is the ��real-time�� ability of the immune system to determine quickly and Deferitrin accurately whether or not a foreign substance is dangerous without having had previous exposure to that antigen. Since peripheral tolerance is one of the most important, yet most poorly understood phenomena associated with immune operation, the GDP interpretation will have profound implications in terms of both interpreting the immune system at a fundamental level and developing improved clinical practices ranging from novel vaccination schemes to treatments for chronic infection and autoimmune diseases. The Growth Detection Paradigm is formulated in reference to the kinetics and signaling interactions in the Treg/ Th17 system. Very generally, after being stimulated by contact with antigens displayed on the surfaces of antigen presenting cells, certain na? ��ve T cells develop into induced Treg cells, which have the ability to suppress an immune response, while others develop into Th17 cells which function as instigators of inflammation, autoimmunity and pathogen defense. With respect to building a dynamics model, two empirical observations regarding Th17 and Treg maturation are of particular importance. First, using a lymphopenic mouse model, the Abbas group has shown that Th17 cells mature rapidly compared to peripheral Treg cells in response to antigenic Dronedarone hydrochloride stimulation. Second, it has been shown that a low concentration of TGF-b is required for Th17 cell survival and/or maturation and that the primary source of this cytokine is the mature Treg cell population. Once Treg cells and Th17 cells have matured, they secrete cytokines that stimulate expansion of their own cell populations, while at the same time inhibiting expansion of the other cell type.