It is therefore not surprising that different people arrive at different solutions with respect to the balance between pathogen defense and propensity towards allergic reaction. Furthermore, based on observations including the hygiene hypothesis, we suggest that while certain immune system parameters might be set by genetics, others are likely tuned during early childhood in Strontium ranelate response to the degree and/or type of antigenic stimulation typically encountered. This tuning during childhood would merely involve slight adjustments to the rates of stimulation, proliferation and turnover of the Treg and Th17 cell populations, and would allow for context specific optimization of the tolerance/ activation thresholds such that a person��s immune system was tailored to the specific range of pathogen growth rates that they might typically encounter during their lifetime. Despite the importance of immune system regulation with respect to pathogen defense, allergic reactions and autoimmunity, an explanation for the generation and maintenance of immune system activation and peripheral tolerance has remained elusive. Most explanations for immune system regulation fall into what we will term the ��missing signals�� category �C these theories suggest that the immune system is triggered to Benzoylmesaconine respond aggressively when it receives several simultaneous signals indicating the presence of a pathogen, but induces tolerance when certain of these multiple signals are absent. While GDP is, essentially, a ��missing signals�� model as well, in GDP the missing signal is not a chemical factor or spatial pattern, but rather, the temporal pattern of growth itself. The GDP model bears some similarity to the model proposed by Steinman and Nussenzweig, who suggested that continued steady state stimulation of T cells by self-antigen presenting immature dendritic cells might tip the immune response towards tolerance. While the steady-state stimulation hypothesis can explain why the immune system does not react towards all antigens, it does not provide a complete explanation for the opposing process of immune activation, particularly as it applies to aggressive immune responses that occur in the absence of any discernable TLR stimulation or other pattern recognition mechanisms.