Elevated serum level of interleukin-32α in the patients with myasthenia gravis

Elevated serum level of interleukin-32α in the patients with myasthenia gravis
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DOI:
10.1007/s00415-011-6036-7
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发表时间:
2011-10-01
影响因子:
6
通讯作者:
Choi, Young-Chul
Choi, Young-Chul
中科院分区:
医学2区
文献类型:
--
作者:
Na, Sang-Jun;So, Seon-Hwa;Choi, Young-Chul

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白细胞介素-32(IL-32)是一种新的细胞因子,在类风湿性关节炎和炎症性肠病等自身免疫性疾病中参与促炎性免疫反应。重症肌无力(MG)是一种针对突触后乙酰胆碱受体(AChR)或神经肌肉接头终板的自身免疫性疾病。IL-32是诱导肿瘤坏死因子(TNF)-α、IL-6、IL-1 β和趋化因子的细胞因子。IL-6、TNF-α和IL-2与MG的发病机制和免疫调节有关。当IL-2或有丝分裂原刺激时,IL-32的基因表达在人自然杀伤(NK)细胞和T淋巴细胞中增加。NK细胞影响实验性自身免疫性MG(EAMG)和可能的MG的发展。本研究的目的是检查MG患者的IL-32 α水平是否升高,并研究IL-32 α水平与人类MG疾病活动性之间的关系。MG患者的血清IL-32 α水平显著较高(p = 0.03):MG患者为460.07 +/- A 192.30 pg/mL,健康对照组为248.45 +/- A 188.42 pg/mL。虽然没有显著的统计学差异,但具有抗AChR结合抗体和阻断抗体的患者的血清IL-32 α水平倾向于高于没有任何抗体的患者(521.56 +/- A 212.92 pg/mL vs. 339.52 +/- A 182.78 pg/mL,p = 0.16)。全身性MG患者血清IL-32 α水平随临床改善而降低。这项研究表明,IL-32可能有助于MG发病机制或免疫调节。
A new cytokine, interleukin-32 (IL-32), has been implicated in the pro-inflammatory immune responses in several autoimmune disorders, such as rheumatoid arthritis and inflammatory bowel diseases. Myasthenia gravis (MG) is a well-characterized autoimmune disease directed at the postsynaptic acetylcholine receptor (AChR) or end plate of the neuromuscular junction. IL-32 is a cytokine that induces tumor necrosis factor (TNF)-alpha, IL-6, IL-1 beta, and chemokine. IL-6, TNF-alpha, and IL-2 are related to the pathogenesis and immunoregulation of MG. The gene expression of IL-32 is increased in human natural killer (NK) cells and T lymphocytes when stimulated by IL-2 or mitogen. NK cells influence the development of experimental autoimmune MG (EAMG) and possibly MG. The aim of this study was to examine whether IL-32 alpha levels are increased in patients with MG and to investigate the relationship between IL-32 alpha levels and disease activity in human MG. Serum IL-32 alpha levels were significantly higher in the MG patients (p = 0.03): 460.07 +/- A 192.30 pg/mL in MG patients and 248.45 +/- A 188.42 pg/mL in the healthy control group. Although there was no significant statistical difference, serum IL-32 alpha levels of patients with both anti-AChR binding and blocking antibodies trended to be higher than those without either antibodies (521.56 +/- A 212.92 pg/mL vs. 339.52 +/- A 182.78 pg/mL, p = 0.16). IL-32 alpha serum levels tended to decrease with clinical improvement in generalized MG. This study suggests the possibility that IL-32 might contribute to MG pathogenesis or immunoregulation.