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   <subfield code="a">10.1007/s00415-011-6036-7</subfield>
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   <subfield code="a">Elevated serum level of interleukin-32α in the patients with myasthenia gravis</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Sang-Jun Na, Seon-Hwa So, Kee Lee, Young-Chul Choi]</subfield>
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   <subfield code="a">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±192.30pg/mL in MG patients and 248.45±188.42pg/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±212.92pg/mL vs. 339.52±182.78pg/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.</subfield>
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   <subfield code="a">Springer-Verlag, 2011</subfield>
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   <subfield code="a">Interleukin-32α (IL-32α)</subfield>
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   <subfield code="a">Myasthenia gravis (MG)</subfield>
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   <subfield code="a">Natural killer cell (NK)</subfield>
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   <subfield code="a">Na</subfield>
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   <subfield code="u">Department of Neurology, Gangnam Severance Hospital, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 146-92 Gangnam-gu, 135-720, Seoul, Republic of Korea</subfield>
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   <subfield code="a">So</subfield>
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   <subfield code="u">Department of Neurology, Gangnam Severance Hospital, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 146-92 Gangnam-gu, 135-720, Seoul, Republic of Korea</subfield>
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   <subfield code="a">Lee</subfield>
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   <subfield code="u">Department of Neurology, Gangnam Severance Hospital, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 146-92 Gangnam-gu, 135-720, Seoul, Republic of Korea</subfield>
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   <subfield code="u">Department of Neurology, Gangnam Severance Hospital, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, 146-92 Gangnam-gu, 135-720, Seoul, Republic of Korea</subfield>
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   <subfield code="g">258/10(2011-10-01), 1865-1870</subfield>
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