Levine S, Saltzman A
Pathology Department, New York Medical College, Valhalla 10595.
J Neuropathol Exp Neurol. 1991 Mar;50(2):126-33. doi: 10.1097/00005072-199103000-00004.
Experimental allergic encephalomyelitis (EAE) was induced in Lewis rats by the injection of spinal cord tissue or myelin basic protein and adjuvants (Freund's or carbonyl iron or pertussis vaccine), or by adoptive immunization. After an interval of five to 12 weeks, the recovered rats were reinoculated by a different route and usually with a different adjuvant. The onset of the second attack was determined by the histologic detection of EAE lesions at intervals during the incubation period. In each of ten experiments, the second attack of EAE occurred one or two days earlier than in naive controls injected at the same time. Residual EAE lesions left over from the first attack could not explain the findings in the reinoculated rats. The accelerated response to the second inoculation may be related to the anamnestic response of classical immunology or to residual damage to the blood-brain barrier. Resistance to a second attack was not encountered in this histopathologic study.
通过注射脊髓组织或髓鞘碱性蛋白及佐剂(弗氏佐剂、羰基铁或百日咳疫苗),或通过过继免疫,在Lewis大鼠中诱导实验性变态反应性脑脊髓炎(EAE)。间隔5至12周后,恢复的大鼠通过不同途径再次接种,且通常使用不同的佐剂。通过在潜伏期每隔一段时间对EAE病变进行组织学检测来确定第二次发作的开始。在十项实验中的每一项中,EAE的第二次发作都比同时注射的未接触过抗原的对照大鼠提前一到两天出现。第一次发作遗留的残余EAE病变无法解释再次接种大鼠的这些发现。对第二次接种的加速反应可能与经典免疫学的回忆反应或血脑屏障的残余损伤有关。在这项组织病理学研究中未发现对第二次发作的抵抗力。