Nicholson S M, Dal Canto M C, Miller S D, Melvold R W
Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, IL 60611, USA.
J Immunol. 1996 Feb 1;156(3):1276-83.
On intracerebral infection with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV), certain mouse strains develop a chronic demyelinating disease similar both clinically and pathologically to human multiple sclerosis. Other strains remain resistant. We previously established that differential susceptibility to this demyelinating disease exists among BALB/c substrains, with BALB/cAnNCr mice being susceptible while BALB/cByJ mice are resistant. BALB/cByJ mice are rendered susceptible to TMEV-induced demyelination on exposure to low dose gamma-irradiation before TMEV infection. BALB/cAnNCr and irradiated, infected BALB/cByJ animals are protected against TMEV-induced demyelination by the transfer of a splenic population from TMEV-infected BALB/cByJ donors. Resistance to demyelination appears to be mediated by a CD8+ radiosensitive population, which is induced on infection with TMEV and which must act early to establish resistance to TMEV-induced demyelination.
在用泰勒鼠脑脊髓炎病毒(TMEV)的BeAn毒株进行脑内感染时,某些小鼠品系会发展出一种慢性脱髓鞘疾病,在临床和病理上都与人类多发性硬化症相似。其他品系则保持抗性。我们之前确定,BALB/c亚系对这种脱髓鞘疾病存在易感性差异,其中BALB/cAnNCr小鼠易感,而BALB/cByJ小鼠具有抗性。BALB/cByJ小鼠在TMEV感染前暴露于低剂量伽马辐射后会变得易受TMEV诱导的脱髓鞘影响。通过从感染TMEV的BALB/cByJ供体转移脾细胞群体,可保护BALB/cAnNCr和经辐射、感染的BALB/cByJ动物免受TMEV诱导的脱髓鞘影响。对脱髓鞘的抗性似乎由一个CD8 +放射敏感群体介导,该群体在感染TMEV时被诱导产生,并且必须在早期发挥作用以建立对TMEV诱导的脱髓鞘的抗性。