特应性支气管哮喘患者急性期康复的免疫学机制。

Gennady V Poryadin, Natalia E Zhuravleva, Jean M Salmasi, Alexander N Kazimirsky, Ludmila Yu Semenova, Sergei A Polner, Tatyana A Chervinskaya
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引用次数: 0

摘要

我们使用多种单克隆抗体对特应性支气管哮喘(ABA)急性期和临床缓解期患者的淋巴细胞表面抗原进行了比较研究。在ABA患者中,独立于疾病的阶段,我们观察到由于辅助T细胞和细胞毒性T细胞这两个亚群的细胞减少,T淋巴细胞总数下降。在疾病的急性期,观察到所有分化阶段的B淋巴细胞数量显著增加。这表明免疫系统的B细胞网络普遍激活。在所有疾病阶段的患者中,我们观察到活化B细胞(CD23+)和早期活化标志物CD25和CD71以及表达粘附受体CD54 (ICAM-1)的淋巴细胞数量的统计学显著升高。相反,血液HLA DR淋巴细胞数量增加两倍仅在疾病的急性期患者中是典型的。在ABA加重期间,CD25/CD95和HLA DR/CD95比值的活化参数显著增加。基于所获得的结果,我们得出结论,ABA缓解的发展与激活诱导的淋巴细胞凋亡的恢复有关,这反过来又导致reagin反应强度的降低。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immunological mechanisms of recovery from an acute stage in patients with atopic bronchial asthma.

We have conducted a comparative study of the lymphocyte surface antigens in patients with atopic bronchial asthma (ABA) in an acute stage and during clinical remission of the disease using a wide variety of monoclonal antibodies. In patients with ABA, independently of the stage of the disease, we have observed a decline in the total number of T lymphocytes due to cell reduction in both sub-populations--T helpers and cytotoxic T cells. During the acute phase of the disease a significant increase in the number of B lymphocytes at all stages of differentiation was observed. This suggests a general activation of the B cell network of the immune system. In patients at all the phases of the disease we observed a statistically significant elevation in the number of activated B cells (CD23+) and of early activation markers CD25 and CD71, as well as of the lymphocytes that express the adhesion receptor CD54 (ICAM-1). On the contrary, a two-fold increase in the number of blood HLA DR lymphocytes was typical only for the patients in an acute phase of the disease. A significant increase in the activation parameters representing the CD25/CD95 and HLA DR/CD95 ratio was found during the ABA aggravation. Based on the obtained results we conclude that the development of the remission in ABA is associated with the restoration of the activation induced apoptosis of the lymphocytes, which in turn leads to a reduction in the intensity of the reagin response.

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