Dolezal J, Fontalin L N, Kondratieva T K, Hraba T
Institute of Information Theory and Automation, Czechoslovak Academy of Sciences, Praha.
Folia Biol (Praha). 1989;35(3):164-70.
Mathematical model of immunological tolerance was applied to polyclonal B cell tolerance induced in mice by treatment with bacterial lipopolysaccharide (LPS) followed by the application of cyclophosphamide (CY). Satisfactory simulation results were obtained with the life-span of lymphocytes shorter than the experimentally observed one. It could be assumed that the massive decrease of lymphocyte population in polyclonal tolerance would elicit a compensatory reaction. Therefore it was postulated that some kind of feedback mechanism increased the influx of B lymphocytes. Having this factor included in the model, satisfactory agreement of the simulation results with experimental data was obtained for experimentally determined life-span of B cells.
将免疫耐受的数学模型应用于通过先用细菌脂多糖(LPS)处理,然后应用环磷酰胺(CY)诱导的小鼠多克隆B细胞耐受。在淋巴细胞寿命短于实验观察到的寿命的情况下获得了令人满意的模拟结果。可以假定多克隆耐受中淋巴细胞群体的大量减少会引发代偿反应。因此推测某种反馈机制增加了B淋巴细胞的流入。将该因素纳入模型后,对于实验确定的B细胞寿命,模拟结果与实验数据获得了令人满意的一致性。