Some pathogen infections and immune system deficiencies have been linked to a few autoimmune diseases. However, the pathogenesis of most autoimmune diseases is unknown. An explanatory hypothesis for the pathogenesis of infection‐initiated autoimmune diseases is provided. Virulent pathogen infections create extensive pathogen antigens that frequently require antibodies. These antibodies create extensive antigen‐antibody immune complexes, which some immuno‐compromised individuals will not adequately eliminate. This will cause inflammatory type III hypersensitivity symptoms, including protease releases that destroy epithelium, mesothelium and endothelium basement membranes, express new immunogenic antigens from previously sequestered basement membrane constituents, and ultimately induce new autoantibodies. This can continue after the infection ends, if the first wave of protease attacks on basement membranes induces new autoantibodies that cause new uncleared antigen‐antibody immune complexes and type III hypersensitivity reactions. The secreted proteases and other enzymes will have preferred substrates and these proteases or other enzymes by themselves, or by their processed protein substrates, can express immunogenic antigens that induce new autoantibodies and initiate various autoimmune diseases. In summary, several autoimmune diseases can be initiated in immuno‐compromised individuals during extensive pathogen infections, if these individuals have two immune problems: (a) slow or weak initial immune responses that result in a reliance on antibodies and (b) an inability to eliminate the resulting antigen‐antibody immune complexes by phagocytosis. These two immune problems and the resulting immune system type III hypersensitivity reaction can explain the causation of several autoimmune diseases, including the most common and the rarest autoimmune diseases, both their differences and their similarities.

中文翻译：

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免疫受损个体中几种自身免疫疾病的发病机理的解释

一些病原体感染和免疫系统缺陷与一些自身免疫性疾病有关。但是，大多数自身免疫性疾病的发病机理尚不清楚。提供了由感染引发的自身免疫性疾病发病机理的解释性假设。强大的病原体感染会产生大量的病原体抗原，这些抗原通常需要抗体。这些抗体可形成广泛的抗原抗体免疫复合物，某些免疫受损的个体无法充分消除这些复合物。这将引起III型炎症反应超敏症状，包括破坏上皮，间皮和内皮基底膜的蛋白酶释放，从先前被隔离的基底膜成分表达新的免疫原性抗原，并最终诱导出新的自身抗体。感染结束后，这种情况可能会继续，如果第一波蛋白酶袭击基膜会诱导新的自身抗体，从而导致新的未清除的抗原抗体免疫复合物和III型超敏反应。分泌的蛋白酶和其他酶将具有优选的底物，这些蛋白酶或其他酶本身或通过其加工的蛋白底物可以表达诱导新的自身抗体并引发各种自身免疫性疾病的免疫原性抗原。总而言之，如果广泛感染的病原体感染有两个免疫问题，则这些免疫受损的个体可能会引发几种自身免疫疾病：（a）慢或弱的初始免疫反应导致对抗体的依赖，以及（b）无法免疫通过吞噬作用消除产生的抗原抗体免疫复合物。