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多发性硬化症患者脑脊液中向CD8 +细胞发出的信号缺失的证据。

Evidence for a missed signal to the CD8+ cells in CSF of multiple sclerosis patients.

作者信息

Saresella M, Grope A, Speciale L, Mancuso R, De Benedictis R, Caputo D, Ferrante P

机构信息

Fondazione Don C. Gnocchi IRCCS, Milano.

出版信息

Ital J Neurol Sci. 1995 Oct;16(7):479-85. doi: 10.1007/BF02229326.

Abstract

Peripheral blood (PB) and cerebrospinal fluid (CSF) lymphocyte subpopulations, defined by various T-cell specific monoclonal antibodies and flow cytometry, were analysed in 44 relapsing remitting multiple sclerosis (RRMS) patients (including 21 subjects in the acute phase and 23 in the stable phase), 40 chronic-progressive multiple sclerosis (CPMS) patients, and 24 patients with other neurological diseases (OND), in order to verify the presence of any abnormality in the lymphocyte subset pattern. A significant increase in the total number of T-lymphocytes and the CD4+ subpopulation was found in the PB of the MS patients in comparison with the OND group. Moreover, a not statistically significant increase in CD4+ cells was observed in the CSF of MS patients. A statistically significant increase was also found in the CD4+ Leu 8+ (suppressor inducer) cells in the CSF of all of the MS groups. Finally, the CD8+ (suppressor/cytotoxic) cell levels, were significantly lower in the CSF of CPMS and stable RMS patients than in the CSF of the OND patients. As a whole, our data suggest that the immunosuppressive deficit that seems to be a constant finding in MS is not due to a decrease in suppressor inducer cell levels, as previously suggested, but may be caused by a missed or altered signal from the suppressor inducer to CD8+ suppressor cells.

摘要

采用多种T细胞特异性单克隆抗体及流式细胞术对44例复发缓解型多发性硬化症(RRMS)患者(包括21例急性期患者和23例稳定期患者)、40例慢性进展型多发性硬化症(CPMS)患者以及24例其他神经系统疾病(OND)患者的外周血(PB)和脑脊液(CSF)淋巴细胞亚群进行分析,以验证淋巴细胞亚群模式中是否存在异常。与OND组相比,MS患者外周血中T淋巴细胞总数及CD4 +亚群显著增加。此外,MS患者脑脊液中CD4 +细胞也有非统计学意义的增加。在所有MS组的脑脊液中,CD4 + Leu 8 +(抑制诱导)细胞也有统计学意义的增加。最后,CPMS患者和稳定期RRMS患者脑脊液中的CD8 +(抑制/细胞毒性)细胞水平显著低于OND患者脑脊液中的水平。总体而言,我们的数据表明,MS中似乎一直存在的免疫抑制缺陷并非如先前所述是由于抑制诱导细胞水平降低所致,而可能是由于抑制诱导细胞向CD8 +抑制细胞发出的信号缺失或改变所致。

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