Serum cytokine and chemokine profiles in patients with myasthenia gravis

Abstract

SummaryMyasthenia gravis (MG) is an autoimmune-mediated inflammatory disease of the neuromuscular junction. Previous studies of animal MG models have suggested important roles of cytokines in MG pathogenesis, but adequate studies on cytokines in human MG are lacking. Using a multiplex suspension array system, we measured the serum levels of 27 cytokines/chemokines in 47 anti-acetylcholine receptor antibody-positive patients with MG and 20 normal controls (NC) to investigate the contribution of cytokines/ chemokines toward MG pathogenesis. Correlations between clinical parameters and cytokine/chemokine levels in patients with MG were also examined. The serum levels of interleukin (IL)-15 (mean ± standard deviation: 6·85 ± 6·97 pg/ml) and vascular endothelial growth factor (VEGF) (96·21 ± 71·60 pg/ml) significantly increased, whereas IL-4 levels (3·57 ± 0·86 pg/ml) decreased in patients with MG compared with NC (IL-15: 4·42 ± 1·55 pg/ml; VEGF: 63·51 ± 32·95 pg/ml; IL-4: 4·15 ± 0·81 pg/ml, P < 0·05). In addition, eight cytokines (IL-4, IL-8, IL-15, eotaxin, macrophage inflammatory protein-1α, macrophage inflammatory protein-1β, VEGF and IL-1b) were significantly changed among MG patients with thymoma, MG patients without thymoma and NC (P < 0·05). Some cytokines, such as IL-4, IL-15, and VEGF, may play roles in the pathogenesis of MG.

Serum high mobility group box 1 is upregulated in myasthenia gravis

“…In this study, patients with MG with thymoma showed higher HMGB1 levels than those without thymoma, which may suggest that HMGB1 is also involved in the pathophysiology of thymus, as reported recently 10. HMGB1 has been shown to stimulate the release of inflammatory cytokines,4 some of which were upregulated in MG 3. Thus, there are potential interactions among these molecules during the inflammatory processes involved in MG pathogenesis.…”

“…Recently, the low-density lipoprotein receptor-related protein 4 (LRP4) antibodies involvement in the pathogenesis of double seronegative MG has been reported 2. T cells, B cells, complement and cytokines play key roles in the pathogenic inflammation in MG 1 3. Inflammation of the neuromuscular junction leads to impaired neuromuscular transmission.…”

An Increase in Circulating B Cell–Activating Factor in Childhood-Onset Ocular Myasthenia Gravis

“…33,34 In this study, no significant difference was observed in the serum levels of IL-17A between pediatric MG patients in the pre-IST period and control subjects, which differed from that in adult MG patients. 31,35 These results suggest an apparent difference in immunological backgrounds between pediatric and adult MG. The absence of coincident increases in serum BAFF and IL-17A levels may be related to negative or low anti-AChR antibody titers in childhood-onset ocular MG.…”

Immunopathogenesis of Myasthenia Gravis (Review)

“…в нервно-мышечных структурах [101,103,115]. В качестве посредников они принимают участие в дифференцировке иммунокомпетентных и гемо-поэтических клеток, в формировании механизмов межклеточного взаимодействия, лежащих в осно-ве иммунного ответа.…”