Agur Z
Department of Applied Mathematics, Weizmann Institute of Science, Rehovot, Israel.
IMA J Math Appl Med Biol. 1987;4(4):295-307. doi: 10.1093/imammb/4.4.295.
Adaptability by means of phenotype variability in host-pathogen systems is studied using a model that resembles a class of array systems known as cellular automata. Each automaton in this model is characterized by a network of n x m processors that process the information contained in levels 0 to m. The effect of the automaton's architecture on its ability to satisfy variations in constraints is analysed, and automata-evolution experiments are described. Increasing the number of organization levels in the automaton is shown to increase its efficiency in buffering external changes, and the mechanism of modulating the processing rules appears more efficient than the mechanism of controlling the mutation rate. Analogy with biological systems suggests that hosts and pathogens evolve towards increasing modulation of their genomic information processing and that single mature lymphocytes should be able to generate more than one antigen receptor. These hypotheses can provide an explanation for the sequential ordered expression of different antigen genes in trypanosomes, as well as for immunosuppression and autoimmune phenomena.
利用一种类似于一类被称为细胞自动机的阵列系统的模型，研究宿主 - 病原体系统中通过表型变异实现的适应性。该模型中的每个自动机由一个n×m处理器网络表征，这些处理器处理0到m级别的信息。分析了自动机架构对其满足约束变化能力的影响，并描述了自动机进化实验。结果表明，增加自动机中的组织级别数量可提高其缓冲外部变化的效率，并且调节处理规则的机制似乎比控制突变率的机制更有效。与生物系统的类比表明，宿主和病原体朝着增加其基因组信息处理的调节方向进化，并且单个成熟淋巴细胞应该能够产生不止一种抗原受体。这些假设可以解释锥虫中不同抗原基因的顺序有序表达，以及免疫抑制和自身免疫现象。
