Disequilibrium of T helper type 1, 2 and 17 cells and regulatory T cells during the development of experimental autoimmune myasthenia gravis

Mu, Lili; Sun, Bo; Kong, Qingfei; Wang, Jinghua; Wang, Guangyou; Zhang, Shujuan; Wang, Dandan; Liu, Yumei; Liu, Yixi; Hui-xia, AN; Li, Hulun

doi:10.1111/j.1365-2567.2009.03089.x

Cited by 89 publications

(72 citation statements)

References 50 publications

(93 reference statements)

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“…Recent data suggest that abnormalities in cellular immunity have an important role in pathogenesis of the disease [10]. In EAMG, the ratio of Th17 cells changes most notably with disease progression accompanied by an upregulated level of IL-17 [16]. But clinical study shows that the frequency of Th17 cells in patients with MG was similar to those in healthy subjects [22].…”

Section: Discussionmentioning

confidence: 99%

“…IL-17 and Th17 cells may play a critical role in coordinating cognate autoreactive T cells and B cells, leading to the genesis of autoantibodies and the subsequent development of EAMG [16]. Despite a growing interest in Th17 cells and their role in the emergence of EAMG, only very limited information is available on the role of this T cell population in the pathogenesis of human MG.…”

Section: Myasthenia Gravis (Mg) Is a Prototypical Cd4mentioning

confidence: 99%

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T Helper Type 17 Cells Expand in Patients with Myasthenia‐Associated Thymoma

Wang¹,

Wang²,

Chen³

et al. 2012

Scand J Immunol

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Myasthenia gravis (MG) is a prototypical CD4+ T cell–dependent autoimmune disease mediated by anti‐acetylcholine receptor autoantibodies (AChR‐Abs). Certain subsets of helper T cells are suggested to be involved in the pathogenesis of MG, including Th1 and regulatory T cells (Treg). However, whether the recently identified Th17 cells play a role in the development of MG and its prognosis is still unknown. Here, we demonstrated that Th17 cells and their associated cytokines are increased, while the Treg cells are decreased in the peripheral blood mononuclear cells (PBMCs) from MG patients with thymomas (TM), but not from those with normal thymus (NT) or thymic hyperplasia (TH). Furthermore, the quantity of Th17 cells correlates with the quantitative myasthenia gravis (QMG) score in patients with TM. We also found a significant positive relationship between the frequency of Th17 cells (%) and the concentration of AChR antibodies in patients with MG. Therefore, the Th17/Treg imbalance in TM may suggest MG with certain pathological subtype, and the increase in Th17 cells may reveal the severity of the disease, which is valuable in the diagnosis and choice of therapeutic strategy for patients with MG.

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Section: Discussionmentioning

confidence: 99%

Section: Myasthenia Gravis (Mg) Is a Prototypical Cd4mentioning

confidence: 99%

T Helper Type 17 Cells Expand in Patients with Myasthenia‐Associated Thymoma

Wang¹,

Wang²,

Chen³

et al. 2012

Scand J Immunol

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“…Previous studies demonstrated that the production of the anti-AChR antibody was T celledependent in MG. [25][26][27][28][29] Th17, a new T-helper subset, is considered to play an important role in the pathophysiology of MG. Mu et al reported that the percentage of Th17 cells to CD4þ cells increased with disease progression and was accompanied by the up-regulation of IL-17 in animal models of autoimmune MG. 30 Zheng et al showed that serum levels of IL-17 were significantly higher in adult patients with MG than in controls. They also demonstrated a positive correlation between circulating IL-17 values and anti-AChR antibody titers in adult MG subjects.…”

Section: Discussionmentioning

confidence: 99%

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

Motobayashi

Inaba

Nishimura

et al. 2015

Pediatric Neurology

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Myasthenia gravis is a B cellemediated autoimmune disorder. The pathophysiology of childhoodonset ocular myasthenia gravis remains unclear. We investigated serum B celleactivating factor levels and other immunological parameters in child patients with ocular myasthenia gravis. METHODS: Blood samples were obtained from 9 children with ocular myasthenia gravis and 20 age-matched controls. We assayed serum concentrations of B celleactivating factor, anti-acetylcholine receptor antibody titers, 7 types of cytokines (interleukins-2, -4, -6, -10, and -17A; interferon-g; tumor necrosis factor-a) as well as the percentages of peripheral blood CD4þ, CD8þ, and CD19þ cells. RESULTS: Serum B celleactivating factor levels were significantly higher before immunosuppressive therapy in patients with childhood-onset ocular myasthenia gravis than in controls and decreased after immunosuppressive therapy. A significant positive correlation was observed between serum B celleactivating factor levels and anti-acetylcholine receptor antibody titers in patients with myasthenia gravis. Serum B celleactivating factor concentrations did not correlate with the percentages of CD4þ, CD8þ, and CD19þ cells or the CD4þ/CD8þ ratio. No significant differences were observed in the levels of the 7 different types of cytokines examined, including interleukin-17A, between preimmunosuppressive therapy myasthenia gravis patients and controls. CONCLUSIONS: Circulating B celleactivating factor may play a key role in the pathophysiology of childhood-onset ocular myasthenia gravis.

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“…In the brain, T reg promote neurotrophic support by inducing astrocytes to increase expression of brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF) (Benner et al 2004;Reynolds et al 2007), and may promote glutamate clearance (Garg et al 2008). Dysfunctional and reduced frequencies of T reg are associated with several autoimmune diseases (Costantino et al 2008), including multiple MS (Venken et al 2008;Fletcher et al 2009;Royal et al 2009;Koen 2010), type 1 diabetes (Glisic et al 2009), inflammatory skin disorders (Fujimura et al 2008), autoimmune myasthenia gravis (Mu et al 2009), and rheumatoid arthritis (Cao et al 2003) as well as chronic inflammatory diseases such as systemic lupus erythematosus (Horwitz 2008;Venigalla et al 2008;Barreto et al 2009), asthma (Xue et al 2007), inflammatory bowel disease (Bourreau et al 2009), and immune dysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome, which is caused by a genetic mutation in the transcription factor FOXP3 (Bennett et al 2001). Furthermore, T reg are being investigated for therapeutic use in several of these diseases (Gonzalez-Rey et al 2006;Brusko et al 2008;Haas et al 2009;Putnam et al 2009;Vandenbark et al 2009).…”

Section: Adaptive Immunity For Therapeutic Gain In Pdmentioning

confidence: 99%