Abstract
We use d'Aspremont and Jacquemin's strategic optimal R&D investment in a duopoly Cournot competition model to construct myopic optimal discrete and continuous R&D dynamics. We show that for some high initial production costs, the success or failure of a firm is very sensitive to small variations in its initial R&D investment strategies.

Abstract
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion are examined by mathematical modelling. We determine the analytic formula that describes the fine balance between Regulatory T cells and T cells at controlled and immune response equilibrium states. We demonstrate that cytokine dependent growth exhibits a quorum T cell population threshold that determines if immune responses develop on activation. We determine the analytic formulas of T cell proliferation thresholds that allow us to study the sensibility of the quorum growth thresholds controlling immune responses.

Abstract
We study a mathematical model of immune response by T cells where the regulatory T cells (Treg) inhibit interleukin 2 secretion. The bystander proliferation to an immune response is modelled. We consider an asymmetry reflecting that the difference between the growth and death rates can be higher for the active T cells and Tregs than for the inactive. This asymmetry leads to a better understanding of the bystander proliferation. An exposure to a pathogen results in an increased proliferation rate of the bystander T cells. If the population of the bystander T cells becomes large enough, autoimmunity can arise, eventually after a long transient period.

Abstract
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion are examined by mathematical modelling. We demonstrate that cytokine dependent growth exhibits quorum T cell population thresholds that determine whether immune responses develop on activation and whether the immune system returns to a control state. We study the effects in the quorum T cell population thresholds, by the T cell maximum growth rate, by the growth rate ratio between Tregs and T cells, by the value of the secretion rate of cytokines, and by the effectiveness of T cell secretion inhibition by Tregs.

Abstract
The consequences of regulatory T cell (Treg) inhibition of interleukine 2 secretion is examined by mathematical modelling. We demonstrate that cytokine dependent growth exhibits a quorum T cell population threshold that determines if immune responses develop on activation. Secretion inhibition manipulates the growth dynamics and effectively increases the quorum threshold, i.e. to develop immune responses a higher number of T cells need to be activated. Thus Treg induced secretion inhibition can provide a mechanism for tissue specific regulation of the balance between suppression (control) and immune responses, a balance that can be varied at the local tissue level through the regulation of the local active Treg population size. However, nonspecific inhibition is prone to escape of initially controlled autoimmune T cells through cross reactivity to pathogens and bystander proliferation on unrelated immune responses.

Abstract
We analyse the effect of the regulatory T cells (Tregs) in the local control of the immune responses by T cells. We obtain an explicit formula for the level of antigenic stimulation of T cells as a function of the concentration of T cells and the parameters of the model. The relation between the concentration of the T cells and the antigenic stimulation of T cells is an hysteresis, that is unfold for some parameter values. We study the appearance of autoimmunity from cross-reactivity between a pathogen and a self antigen or from bystander proliferation. We also study an asymmetry in the death rates. With this asymmetry we show that the antigenic stimulation of the Tregs is able to control locally the population size of Tregs. Other effects of this asymmetry are a faster immune response and an improvement in the simulations of the bystander proliferation. The rate of variation of the levels of antigenic stimulation determines if the outcome is an immune response or if Tregs are able to maintain control due to the presence of a transcritical bifurcation for some tuning between the antigenic stimuli of T cells and Tregs. This behavior is explained by the presence of a transcritical bifurcation.