Potts W K, Slev P R
Department of Pathology, University of Florida, Gainesville 32610-0275, USA.
Immunol Rev. 1995 Feb;143:181-97. doi: 10.1111/j.1600-065x.1995.tb00675.x.
We present six models that are currently the most likely ways that pathogens might favor the evolution of MHC genetic diversity. Although each model makes one or more unique predictions, the current lack of crucial data prevents distinguishing the relative importance of each model. However, this first-time organization of these models should contribute to the design of critical experiments. This synthetic review yields at least three essentially new ideas. First, MHC-dependent immune recognition may be sufficiently redundant to render it essentially escape-proof by pathogens. Second, the four models based on pathogen escape do not work (or work weakly) for diversifying class II genes, unless class II-restricted cytotoxic T-cells are important, an idea that is controversial. Third, pathogen-escape events have traditionally been thought to result in only frequency-dependent selection but here we show that heterozygote advantage is an inevitable consequence of such pathogen evasion. Therefore, the controversy over the relative importance of these two forms of balancing selection is largely a false dichotomy.
我们提出了六种模型，它们目前是病原体可能促进MHC基因多样性进化的最有可能的方式。尽管每个模型都做出了一个或多个独特的预测，但目前缺乏关键数据，无法区分每个模型的相对重要性。然而，这些模型的首次整理应该有助于关键实验的设计。这篇综合性综述至少产生了三个本质上全新的观点。第一，依赖MHC的免疫识别可能足够冗余，以至于病原体基本上无法逃避。第二，基于病原体逃逸的四个模型对II类基因的多样化不起作用（或作用微弱），除非II类限制性细胞毒性T细胞很重要，而这一观点存在争议。第三，传统上认为病原体逃逸事件只会导致频率依赖性选择，但我们在此表明，杂合子优势是这种病原体逃避的必然结果。因此，关于这两种平衡选择形式相对重要性的争议在很大程度上是一种错误的二分法。
