Abstract
For a spatial stochastic epidemic model we investigate in the pair approximation scheme the differential equations for the moments. The basic reinfection model of susceptible-infected-recovered-reinfected or SIRI type is analysed, its phase transition lines calculated analytically in this pair approximation.

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
Previous epidemiological studies on SIS model have only considered the dynamic evolution of the mean value and the variance of the infected individuals. In this paper, through cumulant neglection, we use the dynamic equations of all the moments of infected individuals to develop a recursive method to compute the equilibria manifold of the moment closure ODE's. Specifically, we use the stable equilibria of the moment closure ODE's to obtain good approximations of the quasi-stationary states of the SIS model. This is a crucial step when the quasi-stationary distribution is highly skewed.

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.