The immune system has many adaptive and dynamic components that are regulated to ensure appropriate, precise and rapid response to a foreign pathogen. A delayed or inadequate immune response can lead to prolonged disease, while an excessive or under-regulated response can lead to autoimmunity. The cytokine, interleukin-2 (IL-2) and its receptor IL-2R play an important role in maintaining this balance.The IL-2 receptor transduces pSTAT5 signal through both the intermediate and high affinity receptors, which differ from each other by the presence of CD25 chain in IL-2 receptor. We present experimental data on the kinetics of pSTAT5 signalling through both of the receptors and develop a model that captures this kinetics. We then use this model to parameterize key aspects of two additional models in which we propose and study two different mechanisms by which IL-2 receptor can transduce distinct signals leading to either an activated or a non-activated cell state. We speculate that this initial state differentiation, perhaps enhanced by downstream feedbacks, may eventually lead to differential cell fates.Our result shows that non-linear dynamical models can suggest resolution of a puzzling array of seemingly contradictory experimental results on IL-2 effect on proliferation and differentiation of T-cells.

中文翻译：

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白细胞介素2对免疫反应调节的影响。

免疫系统具有许多适应性和动态成分，可以调节这些成分，以确保对外来病原体做出适当，准确和快速的反应。免疫反应延迟或不足会导致疾病延长，而反应过度或调控不足会导致自身免疫。细胞因子，白介素2（IL-2）及其受体IL-2R在维持这种平衡方面起着重要作用。IL-2受体通过中亲和高亲和力受体转导pSTAT5信号，两者之间存在差异。 IL-2受体中CD25链的存在。我们目前通过两个受体的pSTAT5信号动力学的实验数据，并开发了捕获这种动力学的模型。然后，我们使用该模型对两个其他模型的关键方面进行参数化，在这些模型中我们提议并研究了两种不同的机制，IL-2受体可通过这些机制转导导致激活或未激活细胞状态的不同信号。我们推测这种初始状态分化可能通过下游反馈而增强，最终可能导致细胞分化差异。我们的结果表明，非线性动力学模型可以解决一系列令人困惑的表面活性实验结果，这些结果对IL-2对增殖的影响相互矛盾和T细胞的分化