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在实验性变应性脑脊髓炎的发展和消退过程中,对中枢神经系统中CD4、CD8、细胞间黏附分子-1、血管细胞黏附分子-1和主要组织相容性复合体II类mRNA进行竞争性聚合酶链反应定量分析。

Competitive PCR quantification of CD4, CD8, ICAM-1, VCAM-1, and MHC class II mRNA in the central nervous system during development and resolution of experimental allergic encephalomyelitis.

作者信息

Lindsey J W, Steinman L

机构信息

Department of Neurology and Neurological Sciences, Stanford University Medical Center, CA 94305.

出版信息

J Neuroimmunol. 1993 Nov-Dec;48(2):227-34. doi: 10.1016/0165-5728(93)90196-6.

Abstract

We used competitive polymerase chain reaction to quantify messenger RNA for the lymphocyte antigens CD4 and CD8, the adhesion molecules ICAM-1 and VCAM-1, and the MHC class II I-A molecule in the spinal cords of SJL/J mice at multiple times during the development and resolution of experimental allergic encephalomyelitis (EAE). CD4 and CD8 were not quantifiable at baseline, became detectable at 5 days after immunization, and increased steadily to a peak during clinical disease. I-A increased after CD4 and CD8, but before onset of disease. ICAM-1 and VCAM-1 did not increase until after onset of clinical disease. CD4, CD8, and I-A remained elevated long after recovery from disease. These results suggest that infiltration of CD4 and CD8 cells into the spinal cord and subsequent upregulation of I-A mRNA play an important role in the development of EAE, but reversal of these processes is not necessary for recovery. Upregulation of ICAM-1 and VCAM-1 mRNA does not appear to be important for development of disease.

摘要

我们采用竞争性聚合酶链反应,在实验性自身免疫性脑脊髓炎(EAE)的发病及缓解过程中的多个时间点,对SJL/J小鼠脊髓中淋巴细胞抗原CD4和CD8、黏附分子ICAM-1和VCAM-1以及MHC II类I-A分子的信使核糖核酸进行定量分析。CD4和CD8在基线时无法定量,免疫后5天可检测到,并在临床疾病期间稳步增加至峰值。I-A在CD4和CD8之后增加,但在疾病发作之前。ICAM-1和VCAM-1直到临床疾病发作后才增加。从疾病中恢复后很长时间,CD4、CD8和I-A仍保持升高。这些结果表明,CD4和CD8细胞浸润到脊髓以及随后I-A mRNA的上调在EAE的发病中起重要作用,但恢复并不需要这些过程的逆转。ICAM-1和VCAM-1 mRNA的上调似乎对疾病的发展并不重要。

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