儿童病毒性脑炎中辅助性T细胞1和2介导的免疫应答的相关性

Nadezda L. Vorobyeva, Valentina B. Gervazieva
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引用次数: 0

摘要

这项工作涉及的问题是,由于病毒抗原和髓鞘碱性蛋白的免疫优势区之间的分子模仿,以及随后参与由T辅助细胞1和2介导的反应,病毒触发脱髓鞘过程的机制。特别强调了表明reagin机制在神经病理学发展中起积极作用的新数据,这与作者在多发性硬化症患者体液反应研究中获得的结果相对应。因此,确定髓鞘碱性蛋白存在明显的总IgE和特异性IgE反应,与疾病更严重的临床表现相关。考虑到脱髓鞘的病毒性质,作者研究了免疫反应的一些体液特征,表明T辅助细胞1和2参与急性病毒性脑炎发病的程度。这些特性的测定是用作者开发的原始方法进行的。本研究结果的分析表明,急性病毒性脑炎患儿自身免疫和特应性反应的参与与相应病毒在髓鞘碱性蛋白免疫优势区表现出分子拟态之间存在明显的关系。预后最不利的是风疹、腺病毒和疱疹性脑炎患儿。
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Correlation of Immune Responses Mediated by T Helper 1 and 2 in Children with Viral Encephalitises.

This work deals with the problem concerning the mechanisms of triggering the demyelinating process by viruses as the consequence of molecular mimicry between viral antigens and the immunodominant region of the myelin basic protein with the subsequent involvement of reactions, mediated by T helper cells 1 and 2. Special emphasis is made on the new data indicating that reagin mechanisms play an active role in the development of neuropathology, corresponding to the results obtained by the authors in the study of humoral response in multiple sclerosis patients. Thus, the presence of pronounced total and specific IgE response was established to myelin basic protein, correlating with more severe clinical manifestations of the disease. Taking into account the viral nature of the demyelinization, the authors studied a number of humoral characteristics of immune response, indicating the degree of the involvement of T helper cells 1 and 2 into the pathogenesis of acute viral encephalitises. The determination of these characteristics was carried out with the use of original methods developed by the authors. The analysis of the results obtained in this study revealed the obvious presence of relationship between the involvement of autoimmune and atopic response in children with acute viral encephalitises and the manifestation of molecular mimicry of corresponding viruses with the immunodominant region of myelin basic protein. The most prognostically unfavorable group was the group of children having rubella, adenovirus and herpetic encephalitises.

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