Department of Neurology, Gangnam Severance Hospital, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 146-92 Gangnam-gu, Seoul, 135-720, Republic of Korea.
J Neurol. 2011 Oct;258(10):1865-70. doi: 10.1007/s00415-011-6036-7. Epub 2011 Apr 13.
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)-α, IL-6, IL-1β, and chemokine. IL-6, TNF-α, 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-32α levels are increased in patients with MG and to investigate the relationship between IL-32α levels and disease activity in human MG. Serum IL-32α levels were significantly higher in the MG patients (p = 0.03): 460.07 ± 192.30 pg/mL in MG patients and 248.45 ± 188.42 pg/mL in the healthy control group. Although there was no significant statistical difference, serum IL-32α levels of patients with both anti-AChR binding and blocking antibodies trended to be higher than those without either antibodies (521.56 ± 212.92 pg/mL vs. 339.52 ± 182.78 pg/mL, p = 0.16). IL-32α 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.
一种新的细胞因子白细胞介素-32（IL-32）已被牵涉到几种自身免疫性疾病的促炎免疫反应中，如类风湿关节炎和炎症性肠病。重症肌无力（MG）是一种特征明确的自身免疫性疾病，针对的是神经肌肉接头的突触后乙酰胆碱受体（AChR）或终板。IL-32 是一种诱导肿瘤坏死因子（TNF）-α、IL-6、IL-1β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。当受到 IL-2 或有丝分裂原刺激时，人类自然杀伤（NK）细胞和 T 淋巴细胞的 IL-32 基因表达增加。NK 细胞影响实验性自身免疫性 MG（EAMG）的发展，并可能影响 MG。本研究旨在探讨 MG 患者的 IL-32α 水平是否升高，并研究人类 MG 患者中 IL-32α 水平与疾病活动度的关系。MG 患者的血清 IL-32α 水平显著升高（p=0.03）：MG 患者为 460.07±192.30pg/mL，健康对照组为 248.45±188.42pg/mL。尽管没有显著的统计学差异，但同时具有抗 AChR 结合和阻断抗体的患者的血清 IL-32α 水平趋势高于没有任何一种抗体的患者（521.56±212.92pg/mL 比 339.52±182.78pg/mL，p=0.16）。全身性 MG 患者的 IL-32α 血清水平随着临床改善而趋于下降。本研究表明，IL-32 可能有助于 MG 的发病机制或免疫调节。
