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
中科院分区:
文献类型:
--
作者:
Na, Sang-Jun;So, Seon-Hwa;Choi, Young-Chul
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.