Källén B, Lögdberg L
Immunobiology. 1982;162(1):86-93. doi: 10.1016/S0171-2985(11)80020-3.
The susceptibility to experimental autoimmune encephalomyelitis (EAE) in Lewis (Lew) and Brown Norway (BN) rats was studied in breeding experiments, evaluating EAE from clinical signs of the disease. The Lew strain is highly susceptible, the BN strain is resistant to EAE. F1 hybrids between the strains show an intermediate susceptibility as described by earlier authors. Back-cross experiments verify that susceptibility is inherited in a complex way, at least according to a two-gene model previously suggested. Analysis of the F1 hybrids showed a bi-modal distribution of clinical scores, one group of rats which appear to have the same degree of susceptibility as the Lew strain, and another group with very low susceptibility. Study of F2 rats produced by F1 rats with high or low susceptibility showed that this property was probably not inherited, arguing against a residual heterozygosity in the parental strains. As an alternative hypothetical explanation, the possibility of allogeneic exclusion of genes regulating suppression of EAE is discussed.
在繁殖实验中,通过评估实验性自身免疫性脑脊髓炎(EAE)的临床症状,研究了Lewis(Lew)大鼠和Brown Norway(BN)大鼠对EAE的易感性。Lew品系高度易感,BN品系对EAE具有抗性。如早期作者所述,这两个品系之间的F1杂种表现出中等易感性。回交实验证实,易感性以复杂的方式遗传,至少符合先前提出的双基因模型。对F1杂种的分析显示临床评分呈双峰分布,一组大鼠的易感性程度似乎与Lew品系相同,另一组大鼠的易感性非常低。对高易感性或低易感性F1大鼠所产生的F2大鼠的研究表明,这种特性可能不是遗传的,这与亲本品系中存在残留杂合性的观点相悖。作为另一种假设性解释,讨论了调节EAE抑制的基因发生同种异体排斥的可能性。