小鼠急性自身免疫性脑脊髓炎。II. 易感性由H-2和组胺致敏基因的组合控制。
Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes.
作者信息
Linthicum D S, Frelinger J A
出版信息
J Exp Med. 1982 Jul 1;156(1):31-40. doi: 10.1084/jem.156.1.31.
Abstract
The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2s and H-2q, respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2s or H-2q strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (KsIsD?) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate responder H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 hapotype and histamine sensitivity is required for the development of acute EAE.
摘要
小鼠急性实验性自身免疫性脑脊髓炎（EAE）的表达受多个显性基因控制，即H-2和组胺致敏基因。分别为H-2s和H-2q的SJL/J和SWR/J小鼠易患EAE，且对百日咳博德特氏菌组胺致敏因子（HSF）敏感，该因子可产生血管活性胺超敏反应。其他H-2s或H-2q品系，如A.SW、B10.Q及其他几个品系，不会发生急性EAE，且对百日咳博德特氏菌HSF不敏感。所测试的一个品系DDD（KsIsD?）对HSF敏感，但不会发生EAE（可能是因为它缺乏合适的反应性H-2单倍型）。然而，B10.S和DDD之间的F1杂种对HSF敏感且会发生EAE。急性EAE的诱导期和效应期显然受H-2和HSF基因组合的控制。急性EAE的发生需要正确的H-2单倍型和组胺敏感性相结合。
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