Rose J W, Welsh C T, Hill K E, Houtchens M K, Fujinami R S, Townsend J J
Neurovirology Research Laboratory VAMC, Salt Lake City, UT 84148, USA.
J Neuroimmunol. 1999 Jun 1;97(1-2):110-8. doi: 10.1016/s0165-5728(99)00064-8.
An augmentation of experimental allergic encephalomyelitis (EAE) was observed when monoclonal antibody (mAb) to intercellular adhesion molecule 1 (ICAM-1) was administered after adoptive transfer. Clinical disease was more severe in the ICAM-1 specific mAb-treated EAE mice and included prominent ataxia compared to the PBS-treated controls or Theiler's murine encephalomyelitis virus (TMEV) infected mice treated with ICAM-1 specific mAb. Neuropathologic evaluation demonstrated a distinctly different distribution of lesions in the anti-ICAM-1-treated EAE mice which featured prominent demyelination and inflammation in the cerebellum, brainstem and cerebrum. These structures were minimally involved in the control mice and mAb treatment did not alter the neuropathology in TMEV-infected mice. These results indicate that anti-ICAM-1 can alter trafficking of lymphocytes and mononuclear cells in EAE but not TMEV-induced demyelinating disease.
在过继转移后给予抗细胞间黏附分子1(ICAM-1)单克隆抗体(mAb)时,观察到实验性变应性脑脊髓炎(EAE)有所加重。与用磷酸盐缓冲盐水(PBS)处理的对照小鼠或用ICAM-1特异性mAb处理的感染泰勒氏鼠脑脊髓炎病毒(TMEV)的小鼠相比,用ICAM-1特异性mAb处理的EAE小鼠临床疾病更严重,包括明显的共济失调。神经病理学评估显示,抗ICAM-1处理的EAE小鼠病变分布明显不同,其特征是小脑、脑干和大脑出现明显的脱髓鞘和炎症。这些结构在对照小鼠中受累程度最小,mAb处理未改变TMEV感染小鼠的神经病理学。这些结果表明,抗ICAM-1可改变EAE中淋巴细胞和单核细胞的运输,但不改变TMEV诱导的脱髓鞘疾病。