Warrender Christina, Forrest Stephanie, Segel Lee
Department of Computer Science, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA.
Bull Math Biol. 2004 Nov;66(6):1493-514. doi: 10.1016/j.bulm.2004.02.003.
In this paper, we use both mathematical modeling and simulation to explore homeostasis of peripheral immune system effector cells, particularly alveolar macrophages. Our interest is in the distributed control mechanisms that allow such a population to maintain itself. We introduce a multi-purpose simulator designed to study individual cell responses to local molecular signals and their effects on population dynamics. We use the simulator to develop a model of growth factor regulation of macrophage proliferation and survival. We examine the effects of this form of regulation in the context of two competing hypotheses regarding the source of new alveolar macrophages. In one model, local cells divide to replenish the population; in the other, only cells migrating from circulation divide. We find that either scenario is plausible, although the influx-driven system is inherently more stable. The proliferation-driven system requires lower cell death and efflux rates than the influx-driven system.
在本文中，我们运用数学建模和模拟方法来探究外周免疫系统效应细胞，特别是肺泡巨噬细胞的稳态。我们关注的是使这类细胞群体得以维持自身的分布式控制机制。我们引入了一个多功能模拟器，旨在研究单个细胞对局部分子信号的反应及其对群体动态的影响。我们利用该模拟器建立了一个巨噬细胞增殖和存活的生长因子调节模型。我们在关于新肺泡巨噬细胞来源的两种相互竞争的假设背景下，考察这种调节形式的影响。在一个模型中，局部细胞分裂以补充细胞群体；在另一个模型中，只有从循环中迁移过来的细胞进行分裂。我们发现这两种情况都是合理的，尽管由流入驱动的系统本质上更稳定。与流入驱动的系统相比，增殖驱动的系统需要更低的细胞死亡率和流出率。
