Neutralization of interleukin-9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses

Neutralization of interleukin-9 ameliorates symptoms of experimental autoimmune myasthenia gravis in rats by decreasing effector T cells and altering humoral responses
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白细胞介素 9 的中和可通过减少效应 T 细胞和改变体液反应来改善大鼠实验性自身免疫性重症肌无力的症状

DOI:
10.1111/imm.12322
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发表时间:
2014-11-01
期刊:
影响因子:
6.4
通讯作者:
Li, Hulun
Li, Hulun
中科院分区:
医学2区
文献类型:
--
作者:
Yao, Xiuhua;Kong, Qingfei;Li, Hulun

文献摘要

被引文献

相似文献

白介素9(IL-9)最初被认为是一种2型辅助性T细胞(Th2)相关的细胞因子,通过影响多种细胞类型参与自身免疫反应的调节。然而,最近的研究表明,产生IL-9的CD4(+)T细胞是Th细胞的一个离散亚群,被称为Th9细胞。虽然Th9细胞已被证明在许多疾病中都很重要,但它们在重症肌无力(MG)中的作用尚不清楚。本研究的目的是确定IL-9和Th9细胞是否促进实验性自身免疫性重症肌无力(EAMG)的进展。结果表明,在EAMG的发展过程中,Th9细胞的比例发生了变化,并伴随着IL-9的上调。用抗IL-9抗体阻断IL-9活性可抑制大鼠EAMG相关病理改变,并降低血清抗乙酰胆碱受体抗体水平。IL-9的中和改变了EAMG中Th亚群的分布,减少了Th1细胞的数量,增加了调节性T细胞的数量。应用抗IL-9抗体可能是治疗MG相关疾病或其他T细胞或B细胞介导的自身免疫性疾病的有效策略。
Interleukin-9 (IL-9) was initially thought to be a type 2 T helper (Th2) -associated cytokine involved in the regulation of autoimmune responses by affecting multiple cell types. However, it was recently shown that IL-9-producing CD4(+) T cells represent a discrete subset of Th cells, designated Th9 cells. Although Th9 cells have been shown to be important in many diseases, their roles in myasthenia gravis (MG) are unclear. The aim of this study was to determine whether IL-9 and Th9 cells promote the progression of experimental autoimmune myasthenia gravis (EAMG). The results showed that the percentage of Th9 cells changed during the progression of EAMG, accompanied by an up-regulation of IL-9. Blocking IL-9 activity with antibodies against IL-9 inhibited EAMG-associated pathology in rats and reduced serum anti-acetylcholine receptor IgG levels. Neutralization of IL-9 altered the Th subset distribution in EAMG, reducing the number of Th1 cells and increasing the number of regulatory T cells. Administration of an anti-IL-9 antibody may represent an effective therapeutic strategy for MG-associated pathologies or other T-cell- or B-cell-mediated autoimmune diseases.