Weltman J K, Senft A W
Parasite Immunol. 1981 Summer;3(2):157-63. doi: 10.1111/j.1365-3024.1981.tb00394.x.
Factors governing the sensitization or desensitization of basophils and mast cells are discussed. Mathematical models are proposed which illustrate the effects of rising or falling specific or non-specific IgE titres on the tendency of these cells to degranulate. The models presented are consistent with the hypothesis that fine-tuning of the degranulatory event is achieved by one or more of the following mechanisms: alteration of the number of IgE receptors on the mast cell membrane; displacement of specific anti-schistosomal IgE by anti-other-IgE molecules; clipping or otherwise inactivating mast cell-fixed specific IgE receptor sites so as to render these incapable of binding antigen. Mechanisms proposed may explain how a mast cell population may evolve from highly sensitive to non-reactive allergic states during early and/or chronic periods of schistosomiasis, only to revert to highly sensitive states once again, after the disease has been overcome.
讨论了影响嗜碱性粒细胞和肥大细胞致敏或脱敏的因素。提出了数学模型,该模型说明了特异性或非特异性IgE滴度上升或下降对这些细胞脱颗粒倾向的影响。所提出的模型与以下假设一致:脱颗粒事件的微调是通过以下一种或多种机制实现的:肥大细胞膜上IgE受体数量的改变;抗其他IgE分子取代特异性抗血吸虫IgE;剪切或以其他方式使肥大细胞固定的特异性IgE受体位点失活,从而使其无法结合抗原。所提出的机制可以解释在血吸虫病的早期和/或慢性期,肥大细胞群体如何从高度敏感状态演变为无反应性过敏状态,而在疾病被克服后又如何再次恢复到高度敏感状态。