[改进的光疗方法在皮肤病患者中的临床和流式细胞术结果]。

H Ullrich, W Stolz, S Barlage, K J Lackner, G Rothe, G Schmitz
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引用次数: 0

摘要

在光合作用中,8-甲氧基补骨脂素(8-MOP)被加入到单核细胞浓缩物中,然后被UVA光激活,从而在DNA链之间形成共价键。输注这些不能再复制的修饰细胞似乎可以消除致病性t细胞克隆,并改善患有皮肤t细胞淋巴瘤、移植物抗宿主反应和各种自身免疫性疾病的患者的临床状况。Edelson等人(1987)描述的原始方法经过Andreu等人(1994)提出的以下修改改进:i)通过使用细胞分离器(COBE Spectra)产生更纯净的浓缩物,红细胞吸收UVA光的数量更少。ii)将8-MOP直接应用于收集袋中,避免了因口服千倍剂量和血清水平变化而产生的药物副作用。iii)收集后的浓缩液照射,所有细胞接受相同的照射剂量。我们治疗了2名男性皮肤t细胞淋巴瘤患者,2名女性特应性湿疹患者和1名男性严重脓疱性牛皮癣患者,共123次体外光化学疗法(ECPC)。除了常规的实验室分析外,通过流式细胞术对淋巴细胞亚群进行了详细的表征,以区分t辅助细胞和t抑制细胞及其激活(HLA-DR, cd25), B细胞,NK细胞和单核细胞亚群。还分析了以下可溶性介质:il -2受体和作为急性期反应指标的Il-8、neopterin和Il-1 β。我们观察到良好的临床改善独立于循环血液白细胞的免疫表型无明显趋势。我们的研究结果表明,ECPC效应不是由全身免疫反应介导的,或者在血室中没有测量到。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Clinical and flow cytometry outcome of improved photopheresis methods in dermatologic patients].

In photopheresis, 8-methoxypsoralen (8-MOP) is added to a mononuclear cell concentrate and then activated by UVA light, thus forming covalent bonds between DNA strands. Infusion of these modified cells that are not able to replicate any more seems to lead to the elimination of pathogenic T-cell clones and clinical improvement in patients suffering from cutaneous T-cell lymphoma, graft versus host reactions, and various autoimmune diseases. The original method described by Edelson et al. (1987) was improved by the following modifications proposed by Andreu et al. (1994): i) by using a cell separator (COBE Spectra) that produced purer concentrate with less red blood cells absorbing UVA light. ii) By applying 8-MOP directly into the collection bag, the drug side effects due to the oral application of the thousandfold dose and varying serum levels were avoided. iii) By irradiating the concentrate after collection, all cells received the same irradiation dosage. We treated 2 men with cutaneous T-cell lymphoma, 2 women with atopic eczema and 1 man with severe pustular psoriasis with overall 123 extracorporeal photochemotherapy (ECPC) sessions. In addition to routine laboratory analysis, detailed characterization of lymphocyte subpopulations was carried out by flow cytometry to differentiate T-helper and T-suppressor cells and their activation (HLA-DR, CD 25), B, NK cells, and monocyte subpopulations. The following mediators soluble were analyzed as well: Il-2-receptor and as indicators of acute phase reaction Il-8, neopterin and Il-1 beta. We observed a good clinical improvement independent of no significant trend in the immunological phenotype of circulating blood leukocytes. Our results suggest that ECPC effects are not mediated by a systemic immune response or alternatively are not measured in the blood compartment.

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