[人基孔肯雅热感染后慢性关节炎的生理病理研究]。

M C Jaffar-Bandjee, P Gasque
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引用次数: 0

摘要

基孔肯雅热感染后的慢性关节炎没有特殊的治疗方法。对小鼠的研究证实了成纤维细胞和成肌细胞作为复制病毒的靶细胞,并表明巨噬细胞在涉及多种细胞因子和嵌合因子的先天免疫反应中发挥关键作用。矛盾的是,除了干扰素- γ和il - 12在急性期显著升高外,TH1和TH2细胞因子水平在急性期和慢性期并没有显著升高。患者康复后,il - 12水平恢复正常。相比之下,患有慢性关节炎的患者在PBMC中表现出持续高水平的il - 12和ifn - α。滑膜组织学检查显示关节炎症是由含有病毒物质的巨噬细胞引起的。金属蛋白酶(MMP2)也有助于组织损伤。基孔肯雅病毒通过内源性和外源性途径导致细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Physiopathology of chronic arthritis following chikungunya infection in man].

Chronic arthritis following chikungunya infection has no specific treatment. Studies on mice have confirmed involvement of fibroblasts and myoblasts as target cells replicating the virus and shown that macrophages play a key role in the innate immune response involving multiple cytokines and chimiokines. Paradoxically, TH1 and TH2 cytokine levels do not increase significantly during the acute and chronic phases, with the exception of interferon-gamma and IL12 that rise dramatically during the acute phase. The level of IL12 returns to normal in patients who recover. In contrast, patients who develop chronic arthritis show persistently high IL12 levels along with IFN-alpha within PBMC. Histologic examination of synovia reveals joint inflammation due to macrophages containing viral material. Metallo-protease (MMP2) also contributes to tissue damage. Chikungunya virus leads to apoptosis by both the intrinsic and extrinsic pathways.

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