首页> 外文期刊>Journal of biological regulators and homeostatic agents >Extracorporeal photochemotherapy reduces the severity of Lewis rat experimental allergic encephalomyelitis through a modulation of the function of peripheral blood mononuclear cells
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Extracorporeal photochemotherapy reduces the severity of Lewis rat experimental allergic encephalomyelitis through a modulation of the function of peripheral blood mononuclear cells

机译:体外光化学疗法通过调节外周血单个核细胞的功能来降低Lewis大鼠实验性过敏性脑脊髓炎的严重程度

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摘要

Extra corporeal photochemotherapy (ECP) is an immunomodulating procedure used in several nonneurological diseases which, similarly to multiple sclerosis, are likely to be due to T-cell-mediated autoimmunity and it is probable that ECP can modulate the normal activity of peripheral blood mononuclear cells (PBMC). Using the Lewis rat experimental allergic encephalomyelitis (EAE) model of human multiple sclerosis (MS) we examined the effect of extracorporeal UV-A irradiation on psoralen-activated PBMC. In our experiment the comparison between the two groups of animals (ECP or sham-treatment) evidenced that the ECP treatment reduced the severity of EAE on clinical grounds and this result was confirmed by the pathological examination. The changes in the titers of anti-myelin antigen antibodies typical of EAE were also modulated by the procedure. Ex vivo examination evidenced a significant reduction in tumor-necrosis factor-α (TNF-α) released by PBMC after lipopolysaccharides (LPS) stimulation in culture. We conclude that ECP modifies the normal activity of PBMC during the course of EAE and it is possible that one of the anti-inflammatory mechanisms of action of ECP is correlated to a down-regulation of T-helper 1 lymphocytes activity.
机译:额外的光化学疗法(ECP)是一种免疫调节程序,用于多种非神经系统疾病,与多发性硬化症类似,可能是由于T细胞介导的自身免疫所致,ECP可能调节外周血单核细胞的正常活动(PBMC)。使用人类多发性硬化症(MS)的Lewis大鼠实验性变应性脑脊髓炎(EAE)模型,我们检查了体外UV-A照射对补骨脂素激活的PBMC的影响。在我们的实验中,两组动物(ECP或假治疗)之间的比较证明,ECP治疗可从临床角度降低EAE的严重程度,并且病理检查证实了这一结果。该程序还调节了EAE典型的抗髓磷脂抗原抗体的效价变化。体外检查表明,培养物中脂多糖(LPS)刺激后,PBMC释放的肿瘤坏死因子-α(TNF-α)明显减少。我们得出结论,ECP在EAE过程中会改变PBMC的正常活性,并且ECP的抗炎机制之一可能与T辅助1淋巴细胞活性的下调有关。

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