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营养不良儿童针对肠道寄生虫蛔虫的保护性IgE反应调节缺陷。

Defective regulation of the protective IgE response against intestinal helminth Ascaris lumbricoides in malnourished children.

作者信息

Hagel I, Lynch N R, Puccio F, Rodriguez O, Luzondo R, Rodríguez P, Sánchez P, Cabrera C M, Di Prisco M C

机构信息

Institute of Biomedicine, Faculty of Medicine, Central University of Venezuela, Caracas, Venezuela.

出版信息

J Trop Pediatr. 2003 Jun;49(3):136-42. doi: 10.1093/tropej/49.3.136.

DOI:10.1093/tropej/49.3.136
PMID:12848201
Abstract

It is well established that malnutrition affects the immune response and increases the susceptibility to parasitic infection. In the present study we evaluated some aspects of the cellular and cytokine network that regulate the IgE responses, which are important components of host defence mechanisms against helminthic parasites in children infected with the intestinal helminth Ascaris lumbricoides, and with differing degrees of malnutrition. We found a defective T cell response in malnourished children, as indicated by diminished levels of circulating total (CD3+), helper (CD4+), IL-2-receptor-bearing (CD4+CD25+) and memory helper T cell responses (CD4+CD45RO+) in keeping with the decreased specific IgE levels against Ascaris lumbricoides. In contrast, the proportions of total B cells (CD20+), and those bearing the low-affinity IgE receptor (CD23+) were increased in the moderated malnourished children. Moreover, serum IL-4 levels and total IgE were also increased in these children. We suggest that malnutrition can cause an imbalance in T cell subpopulations that may lead to a defective T cell maturation and a decreased specific anti-Ascaris IgE response thus increasing the susceptibility to such infections. The high levels of total IgE observed may be related to a non-specific stimulation of the proliferation of activated B cells, probably caused by helminthic parasites and other infectious agents that are frequent in malnourished children.

摘要

营养不良会影响免疫反应并增加对寄生虫感染的易感性,这一点已得到充分证实。在本研究中,我们评估了细胞和细胞因子网络的某些方面,这些方面调节IgE反应,而IgE反应是感染肠道蛔虫(蛔虫)且营养不良程度不同的儿童抵御蠕虫寄生虫的宿主防御机制的重要组成部分。我们发现营养不良儿童的T细胞反应存在缺陷,这表现为循环中总T细胞(CD3+)、辅助性T细胞(CD4+)、表达IL-2受体的T细胞(CD4+CD25+)和记忆辅助性T细胞反应(CD4+CD45RO+)水平降低,这与针对蛔虫的特异性IgE水平降低一致。相比之下,中度营养不良儿童的总B细胞(CD20+)以及表达低亲和力IgE受体的B细胞(CD23+)比例增加。此外,这些儿童的血清IL-4水平和总IgE也升高。我们认为,营养不良会导致T细胞亚群失衡,这可能会导致T细胞成熟缺陷以及特异性抗蛔虫IgE反应降低,从而增加对这类感染的易感性。观察到的总IgE高水平可能与活化B细胞增殖的非特异性刺激有关,这可能是由营养不良儿童中常见的蠕虫寄生虫和其他感染因子引起的。

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