Blank Miri, Barzilai Ori, Shoenfeld Yehuda
The Center for Autoimmune Diseases, Department of Medicine 'B', Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Israel.
Clin Rev Allergy Immunol. 2007 Feb;32(1):111-8. doi: 10.1007/BF02686087.
The term "molecular mimicry" was coined by R. Damian in 1964, who was first to suggest that antigenic determinants of micro-organisms may resemble antigenic determinants of their host. Damian suggested that this similarity served as a defense mechanism of a microorganism from the host's immune system and prevented the development of immune response to the micro-organism, thereby protecting it from host defense. Years later, the term "molecular mimicry" was attributed a different meaning-namely, antigenic determinants of microorganisms might elicit an auto-immune response that harms the host. The concept of molecular mimicry is based on a structural similarity between a pathogen or metabolite and self-structures. The similarity could be expressed as shared amino acid sequences (linear or mimotope) or similar conformational structure between a pathogen and self-antigen. "Molecular mimicry" has become a very popular explanation for the frequent association of infection with auto-immune disease.
“分子模拟”一词由R. 达米安于1964年创造,他首次提出微生物的抗原决定簇可能类似于其宿主的抗原决定簇。达米安认为这种相似性是微生物抵御宿主免疫系统的一种防御机制,可阻止对该微生物产生免疫反应,从而保护其免受宿主防御。多年后,“分子模拟”一词被赋予了不同的含义,即微生物的抗原决定簇可能引发损害宿主的自身免疫反应。分子模拟的概念基于病原体或代谢产物与自身结构之间的结构相似性。这种相似性可以表现为共享的氨基酸序列(线性或模拟表位),或者病原体与自身抗原之间相似的构象结构。“分子模拟”已成为感染与自身免疫性疾病频繁关联的一种非常流行的解释。