T cell infiltration after chronic constriction injury of mouse sciatic nerve is associated with interleukin-17 expression

T cell infiltration after chronic constriction injury of mouse sciatic nerve is associated with interleukin-17 expression
复制标题

DOI:
10.1016/j.expneurol.2006.03.014
复制
发表时间:
2006-08-01
影响因子:
5.3
通讯作者:
Stoll, Guido
Stoll, Guido
中科院分区:
医学2区
文献类型:
--
作者:
Kleinschnitz, Christoph;Hofstetter, Harald H.;Stoll, Guido

文献摘要

被引文献

相似文献

白细胞介素17A(IL-17A)是最近发现的一种新的T细胞细胞因子,可在多种免疫介导性疾病中协调炎症反应。本研究采用定量逆转录聚合酶链式反应(qRT-PCR)技术,分析了小鼠坐骨神经慢性压迫性损伤(CCI)后IL-17A及其主要调控因子IL-23和IL-15的表达模式。在CCI后第7天,IL-17A在变性神经中呈单相表达,而IL-17A调节细胞因子IL-23和IL-15的转录较早达到峰值。相应地,免疫细胞化学显示损伤神经内膜内可检测到IL-17A阳性T细胞。为了支持T细胞炎症的关键作用,缺乏功能性T淋巴细胞的RAG-1基因敲除小鼠在CCI后的远端神经节段不表达IL-17A mRNA。有趣的是,T细胞缺陷与CCI后热痛觉过敏减轻以及巨噬细胞标志分子F4/80和趋化因子巨噬细胞趋化蛋白-1(MCP-1)的mRNA水平降低有关。我们的研究支持T细胞和T细胞衍生的细胞因子参与周围神经损伤后的炎症反应的观点。(C)2006 Elsevier Inc.保留所有权利。
Interleukin (IL)-17A, a recently described novel T cell cytokine, orchestrates inflammation in a variety of immune-mediated diseases. In the present investigation, we analyzed the temporal gene expression pattern of IL-17A and its main regulators IL-23 and IL-15 after chronic constriction injury (CCI) of the sciatic nerve, a lesion paradigm inducing neuropathic pain, by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in mice. IL-17A displayed a monophasic expression in degenerating nerves at day 7 after CCI while transcripts for the IL-17A regulatory cytokines IL-23 and IL-15 peaked earlier. Accordingly, IL-17A positive T cells were detectable within the endoneurium of the injured nerves by immunocytochemistry. In support of a crucial role of T cell inflammation, RAG-1 knockout mice lacking functional T lymphocytes did not express IL-17A mRNA in distal nerve segments following CCI. Interestingly, T cell deficiency was associated with less thermal hyperalgesia and reduced mRNA levels for the macrophage marker molecule F4/80 and the chemokine macrophage chemoattractant protein-1 (MCP-1) after CCI. Our study supports the notion that T cells and T-cell-derived cytokines contribute to the inflammatory response after peripheral nerve injury. (c) 2006 Elsevier Inc. All rights reserved.