Munoz J J, Mackay I R
J Neuroimmunol. 1984 Dec;7(2-3):91-6. doi: 10.1016/s0165-5728(84)80009-0.
Strains of mice (BALB/c An Bradley/Wehi, C57B1/10J, CBA/ca H Wehi, DBA/2 Wf, A/J Wehi), thought to be genetically resistant to experimental allergic encephalomyelitis (EAE) and known to be resistant to becoming hypersensitive to histamine after administration of pertussis vaccine were tested for their ability to develop EAE when purified pertussigen was included in the immunization. It was found that C57B1/10J, CBA/ca H Wehi, BALB/c An Bradley/Wehi and DBA/2 Wf developed typical signs and histologic evidence of EAE. The A/J Wehi and the B10D2/n Sn (not previously tested) strains developed only mild signs of EAE, while the known susceptible (SJL/J X BALB/c An Bradley/Wehi) F1 hybrids developed severe EAE. Histologic evidence of EAE was lacking in A/J Wehi mice and was minimal in B10D2/n Sn mice. These results suggest that neither the H-2 complex nor the gene controlling susceptibility to sensitization to histamine by administration of pertussigen are wholly responsible for susceptibility to EAE.
人们认为某些品系的小鼠(BALB/c An Bradley/Wehi、C57B1/10J、CBA/ca H Wehi、DBA/2 Wf、A/J Wehi)对实验性变应性脑脊髓炎(EAE)具有遗传抗性,并且已知在接种百日咳疫苗后对组胺不会变得过敏。当免疫接种中包含纯化的百日咳杆菌抗原时,对这些小鼠产生EAE的能力进行了测试。结果发现,C57B1/10J、CBA/ca H Wehi、BALB/c An Bradley/Wehi和DBA/2 Wf出现了EAE的典型症状和组织学证据。A/J Wehi和B10D2/n Sn品系(之前未测试过)仅出现了EAE的轻微症状,而已知易感的(SJL/J×BALB/c An Bradley/Wehi)F1杂交种则出现了严重的EAE。A/J Wehi小鼠缺乏EAE的组织学证据,B10D2/n Sn小鼠的组织学证据最少。这些结果表明,H-2复合体和控制因接种百日咳杆菌抗原而对组胺致敏易感性的基因都不能完全解释对EAE的易感性。