Elevated serum level of interleukin-32α in the patients with myasthenia gravis
- First Online:
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.
KeywordsInterleukin-32α (IL-32α) Autoimmune disorder Myasthenia gravis (MG) Natural killer cell (NK)
- 12.Netea MG, Azam T, Ferwerda G, Girardin SE, Walsh M, Park JS, Abraham E, Kim JM, Yoon DY, Dinarello CA, Kim SH (2005) IL-32 synergizes with nucleotide oligomerization domain (NOD) 1 and NOD2 ligands for IL-1beta and IL-6 production through a caspase 1-dependent mechanism. Proc Natl Acad Sci USA 102:16309–16314PubMedCrossRefGoogle Scholar