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https://www.readbyqxmd.com/read/29759142/heterogeneity-of-auto-antibodies-against-nachr-in-myasthenic-serum-and-their-pathogenic-roles-in-experimental-autoimmune-myasthenia-gravis
#1
Ryuichi Nakamura, Tomohiro Makino, Takeshi Hanada, Maki Terakawa, Kazuhiro Nagahira, Jyoji Yamate, Hirokazu Shiraishi, Masakatsu Motomura
Many myasthenia gravis (MG) patients have auto-antibodies against the nicotinic acetylcholine receptor (nAChR), and monoclonal antibodies against the main immunogenic region (MIR) of nAChR can induce experimental autoimmune MG (EAMG). We investigated whether Fab fragment of MIR antibody (Fab35) could block the pathogenicity of polyclonal antibodies. Fab35 partially inhibited nAChR downmodulation, blocked EAMG serum-induced binding of polyclonal antibodies and complement deposition in vitro. Moreover, Fab35 did not ameliorate the EAMG serum-induced EAMG phenotype in rats...
July 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29568889/treatment-of-experimental-autoimmune-myasthenia-gravis-rats-with-fty720-and-its-effect-on-th1-th2-cells
#2
Jiankang Huang, Ting Zhang, Hongmei Wang, Yuwu Zhao
Myasthenia gravis (MG) is an autoimmune neurological disease that is characterized by the expression of anti-acetylcholine receptor (AChR) antibodies. The immune response at AChRs of neuromuscular junction is disrupted in patients with MG, which manifests as skeletal muscle fatigue and is aggravated following periods of activity and alleviated following rest. Although a novel immune suppressant FTY720 drug, which exhibits strong immune suppression efficacy and minor adverse effects, is available, its role and mechanism in MG have not been elucidated...
March 16, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29421431/introducing-autoimmunity-at-the-synapse-by-a-novel-animal-model-of-experimental-autoimmune-myasthenia-gravis
#3
REVIEW
Jianwen Wang, Yatao Xiao, Kejing Zhang, Benyan Luo, Chengyong Shen
The neuromuscular junction (NMJ) is a peripheral synapse between motor neurons and skeletal muscle fibers that controls muscle contraction. The NMJ is the target of various disorders including myasthenia gravis (MG), an autoimmune disease in which auto-antibodies (auto-Abs) attack the synapse, and thus cause muscle weakness in patients. There are multiple auto-Abs in the MG patient sera, but not all the Abs are proven to be pathogenic, which increases the difficulties in clinical diagnoses and treatments. To establish the causative roles of auto-Abs in MG pathogenesis, the experimental autoimmune MG (EAMG) induced by the active immunization of auto-antigens (auto-Ags) or the passive transfer of auto-Abs is required...
March 15, 2018: Neuroscience
https://www.readbyqxmd.com/read/29377167/acetylcholine-receptor-specific-immunosuppressive-therapy-of-experimental-autoimmune-myasthenia-gravis-and-myasthenia-gravis
#4
REVIEW
Jie Luo, Jon Lindstrom
Experimental autoimmune myasthenia gravis (EAMG) and myasthenia gravis (MG) are caused by autoantibodies to the extracellular domain of muscle nicotinic acetylcholine receptors (AChRs). Autoantibodies to the cytoplasmic domain of AChRs do not cause EAMG because they cannot bind AChRs in vivo. The ideal MG therapy would quickly and permanently suppress only the pathological autoimmune response to AChRs. We have developed a specific immunosuppressive therapy for EAMG that involves immunizing rats with bacterially expressed cytoplasmic domains of human muscle AChRs...
February 2018: Annals of the New York Academy of Sciences
https://www.readbyqxmd.com/read/29331804/toll-like-receptor-9-antagonist-suppresses-humoral-immunity-in-experimental-autoimmune-myasthenia-gravis
#5
Peng Zhang, Chun-Lin Yang, Ru-Tao Liu, Heng Li, Min Zhang, Na Zhang, Long-Tao Yue, Cong-Cong Wang, Ying-Chun Dou, Rui-Sheng Duan
Recent studies have demonstrated the important role of toll-like receptor 9 (TLR9) signalling in autoimmune diseases, but its role in myasthenia gravis (MG) has not been fully established. We show herein that blocking TLR9 signalling via the suppressive oligodeoxynucleotide (ODN) H154 alleviated the symptoms of experimental autoimmune myasthenia gravis (EAMG). With the downregulation of dendritic cells (DCs), TLR9 interruption reduced follicular helper T cells (Tfh) and germinal centre (GC) B cells, leading to decreased antibody production...
February 2018: Molecular Immunology
https://www.readbyqxmd.com/read/29205338/s1p-receptor-antagonists-fingolimod-and-siponimod-do-not-improve-the-outcome-of-experimental-autoimmune-myasthenia-gravis-mice-after-disease-onset
#6
Andreas Pelz, Hanne Schaffert, Radharani Diallo, Falk Hiepe, Andreas Meisel, Siegfried Kohler
Myasthenia gravis (MG) is an autoimmune disease characterized by muscle weakness and fatigue in the presence of circulating antibodies against components of the neuromuscular junction. Most patients have a good prognosis, but some are refractory to standard-of-care immunosuppressive treatment and suffer from recurrent myasthenic crises. Functional sphingosine-1-phosphate (S1P) antagonists like fingolimod and siponimod (BAF312) are successfully used for the treatment of multiple sclerosis, and fingolimod was shown to prevent the development of myasthenic symptoms in experimental autoimmune myasthenia gravis (EAMG), the standard model of MG...
March 2018: European Journal of Immunology
https://www.readbyqxmd.com/read/29193204/engineered-agrin-attenuates-the-severity-of-experimental-autoimmune-myasthenia-gravis
#7
Zhiguo Li, Minshu Li, Kristofer Wood, Steffan Hettwer, Suraj A Muley, Fu-Dong Shi, Qiang Liu, Shafeeq S Ladha
INTRODUCTION: Agrin is essential for the formation and maintenance of neuromuscular junctions (NMJs). NT-1654 is a C-terminal fragment of mouse neural agrin. In this study, we determined the effects of NT-1654 on the severity of experimental autoimmune myasthenia gravis (EAMG). METHODS: EAMG was induced in female Lewis rats by immunization with the Torpedo acetylcholine receptor (tAChR) and complete Freund's adjuvant (CFA). NT-1654 was dissolved in phosphate-buffered saline (PBS) and injected daily subcutaneously into tAChR immunized rats during the first 10 days after immunization, and then every other day for the following 20 days...
November 28, 2017: Muscle & Nerve
https://www.readbyqxmd.com/read/28972088/nfat1-regulates-systemic-autoimmunity-through-the-modulation-of-a-dendritic-cell-property
#8
Chang-Suk Chae, Gi-Cheon Kim, Eun Sil Park, Choong-Gu Lee, Ravi Verma, Hagg-Lim Cho, Chang-Duk Jun, Yung Joon Yoo, Sin-Hyeog Im
The transcription factor NFAT1 plays a pivotal role in the homeostasis of T lymphocytes. However, its functional importance in non-CD4+ T cells, especially in systemic immune disorders, is largely unknown. In this study, we report that NFAT1 regulates dendritic cell (DC) tolerance and suppresses systemic autoimmunity using the experimental autoimmune myasthenia gravis (EAMG) as a model. Myasthenia gravis and EAMG are T cell-dependent, Ab-mediated autoimmune disorders in which the acetylcholine receptor is the major autoantigen...
November 1, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28959261/a-novel-approach-to-reinstating-tolerance-in-experimental-autoimmune-myasthenia-gravis-using-a-targeted-fusion-protein-mcta1-t146
#9
Alessandra Consonni, Sapna Sharma, Karin Schön, Cristina Lebrero-Fernández, Elena Rinaldi, Nils Yngve Lycke, Fulvio Baggi
Reinstating tissue-specific tolerance has attracted much attention as a means to treat autoimmune diseases. However, despite promising results in rodent models of autoimmune diseases, no established tolerogenic therapy is clinically available yet. In the experimental autoimmune myasthenia gravis (EAMG) model several protocols have been reported that induce tolerance against the prime disease-associated antigen, the acetylcholine receptor (AChR) at the neuromuscular junction. Using the whole AChR, the extracellular part or peptides derived from the receptor, investigators have reported variable success with their treatments, though, usually relatively large amounts of antigen has been required...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28844501/onx-0914-a-selective-inhibitor-of-immunoproteasome-ameliorates-experimental-autoimmune-myasthenia-gravis-by-modulating-humoral-response
#10
Ru-Tao Liu, Peng Zhang, Chun-Lin Yang, Yu Pang, Min Zhang, Na Zhang, Long-Tao Yue, Xiao-Li Li, Heng Li, Rui-Sheng Duan
Accumulating evidence shows that the immunoproteasome participates in the immune response, beyond its initial role in the protein degradation. Here, we tested the effects of the selective immunoproteasome inhibitor, ONX-0914, on experimental autoimmune myasthenia gravis (EAMG). We found that ONX-0914 ameliorated the severity of ongoing EAMG by reducing the autoantibody affinity, accompanied with decreased Tfh cells and antigen presenting cells. Also it reduced the percentage of Th17 cells and inhibited the secretion of IL-17...
October 15, 2017: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/28833081/transcriptional-repressor-blimp1-regulates-follicular-regulatory-t-cell-homeostasis-and-function
#11
Guang Yang, Xiaosu Yang, Junmei Zhang, Guancheng Li, Dandan Zheng, Anjiao Peng, Jue Hu, Liqun Xu, Baifeng Yang, Huan Yang, Wenbin Zhou, Erdem Tuzun, Jing Li
The B-lymphocyte-induced maturation protein 1 (Blimp1) regulates T-cell homeostasis and function. Loss of Blimp1 could double the proportion of follicular regulatory T (Tfr) cells. However, the effects that Blimp1 may have on the function of Tfr cells remain unknown. Here we document the function for Blimp1 in Tfr cells in vitro and in vivo. Data presented in this study demonstrate that Tfr cells indirectly inhibit the activation and differentiation of B cells by negatively regulating follicular helper T cells, so lowering the secretion of antibody...
January 2018: Immunology
https://www.readbyqxmd.com/read/28822831/ifna-as1-regulates-cd4-t-cell-activation-in-myasthenia-gravis-though-hla-drb1
#12
Mengchuan Luo, Xiaofang Liu, Huanyu Meng, Liqun Xu, Yi Li, Zhibin Li, Chang Liu, Yue-Bei Luo, Bo Hu, Yuanyuan Xue, Yu Liu, Zhaohui Luo, Huan Yang
Abnormal CD4+ T cell activation is known to play roles in the pathogenesis of myasthenia gravis (MG). However, little is known about the mechanisms underlying the roles of lncRNAs in regulating CD4+ T cell. In this study, we discovered that the lncRNA IFNG-AS1 is abnormally expressed in MG patients associated with quantitative myasthenia gravis (QMG) and the positive anti-AchR Ab levels patients. IFNG-AS1 influenced Th1/Treg cell proliferation and regulated the expression levels of their transcription factors in an experimental autoimmune myasthenia gravis (EAMG)model...
October 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/28756524/muscle-satellite-cells-are-functionally-impaired-in-myasthenia-gravis-consequences-on-muscle-regeneration
#13
Mohamed Attia, Marie Maurer, Marieke Robinet, Fabien Le Grand, Elie Fadel, Rozen Le Panse, Gillian Butler-Browne, Sonia Berrih-Aknin
Myasthenia gravis (MG) is a neuromuscular disease caused in most cases by anti-acetyl-choline receptor (AChR) autoantibodies that impair neuromuscular signal transmission and affect skeletal muscle homeostasis. Myogenesis is carried out by muscle stem cells called satellite cells (SCs). However, myogenesis in MG had never been explored. The aim of this study was to characterise the functional properties of myasthenic SCs as well as their abilities in muscle regeneration. SCs were isolated from muscle biopsies of MG patients and age-matched controls...
December 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/28743581/caspase-1-inhibitor-regulates-humoral-responses-in-experimental-autoimmune-myasthenia-gravis-via-il-6-dependent-inhibiton-of-stat3
#14
Cong-Cong Wang, Min Zhang, Heng Li, Xiao-Li Li, Long-Tao Yue, Peng Zhang, Ru-Tao Liu, Hui Chen, Yan-Bin Li, Rui-Sheng Duan
We have previously demonstrated that Cysteinyl aspartate-specific proteinase-1 (caspase-1) inhibitor ameliorates experimental autoimmune myasthenia gravis (EAMG) by inhibited cellular immune response, via suppressing DC IL-1 β, CD4(+) T and γdT cells IL-17 pathways. In this study, we investigated the effect of caspase-1 inhibitor on humoral immune response of EAMG and further explore the underlying mechanisms. An animal model of MG was induced by region 97-116 of the rat AChR α subunit (R97-116 peptide) in Lewis rats...
July 22, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28655853/rapamycin-alleviates-inflammation-and-muscle-weakness-while-altering-the-treg-th17-balance-in-a-rat-model-of-myasthenia-gravis
#15
Feng Jing, Fei Yang, Fang Cui, Zhaohui Chen, Li Ling, Xusheng Huang
Myasthenia gravis (MG) is an autoimmune disease commonly treated with immunosuppressants. We evaluated the novel immunosuppressant, rapamycin (RAPA), in a rat model of experimental autoimmune MG (EAMG). Mortality rates in the RAPA (12%) were significantly down compared with the EAMG (88%) or cyclophosphamide (CTX) (68%) intervention groups. Muscular weakness decreased after both RAPA and CTX treatment. However, Lennon scores were lower (1.74 ± 0.49, 3.39 ± 0.21, and 3.81 ± 0.22 in RAPA, CTX, and EAMG groups, respectively), and body weights (203...
August 31, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28599652/regulatory-t-cells-in-multiple-sclerosis-and-myasthenia-gravis
#16
REVIEW
K M Danikowski, S Jayaraman, B S Prabhakar
Multiple sclerosis (MS) is a chronic debilitating disease of the central nervous system primarily mediated by T lymphocytes with specificity to neuronal antigens in genetically susceptible individuals. On the other hand, myasthenia gravis (MG) primarily involves destruction of the neuromuscular junction by antibodies specific to the acetylcholine receptor. Both autoimmune diseases are thought to result from loss of self-tolerance, which allows for the development and function of autoreactive lymphocytes. Although the mechanisms underlying compromised self-tolerance in these and other autoimmune diseases have not been fully elucidated, one possibility is numerical, functional, and/or migratory deficits in T regulatory cells (Tregs)...
June 9, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28599246/ablation-of-il-17-expression-moderates-experimental-autoimmune-myasthenia-gravis-disease-severity
#17
Gabriela Aguilo-Seara, Yanchen Xie, Jarrod Sheehan, Linda L Kusner, Henry J Kaminski
An array of cytokines influences the pathogenesis of early onset myasthenia gravis (MG) and its animal model, experimental autoimmune myasthenia gravis (EAMG). Patients with MG, in particular those with more severe weakness, have elevations of the pro-inflammatory cytokine IL-17 in the blood. We assessed the role of IL-17A in autoimmunity by inducing EAMG in mice with knockout of IL-17 and found a reduction of EAMG severity, but not a complete ablation of disease. The IL-17ko mice had no evidence of weakness, low levels of acetylcholine receptor antibodies, and retention of acetylcholine receptor at the neuromuscular junction...
August 2017: Cytokine
https://www.readbyqxmd.com/read/28548588/injection-of-inactive-bordetella-pertussis-and-complete-freund-s-adjuvant-with-torpedo-californica-achr-increases-the-occurrence-of-experimental-autoimmune-myasthenia-gravis-in-c57bl-6-mice
#18
Takahiro Maruta, Minako Oshima, Dennis R Mosier, M Zouhair Atassi
An animal model of myasthenia gravis (MG), termed experimental autoimmune MG (EAMG), is an important tool for investigations of disease mechanisms and/or methods of treatment for this disease. EAMG can be induced in C57BL/6 (B6, H-2(b)) mice by 2-3 times injections at 4 weeks intervals with Torpedo californica (t) acetylcholine receptor (AChR) in complete Freund's adjuvant (CFA). However, the protocol especially with a two-injection schedule occasionally produces a poor incidence of EAMG. We have investigated the efficacy of the additional adjuvant, inactive organisms of Bordetella pertussis (iBP), on the induction with a two-injection schedule...
May 26, 2017: Autoimmunity
https://www.readbyqxmd.com/read/28523463/immature-exosomes-derived-from-microrna-146a-overexpressing-dendritic-cells-act-as-antigen-specific-therapy-for-myasthenia-gravis
#19
Weifan Yin, Song Ouyang, Zhaohui Luo, Qiuming Zeng, Bo Hu, Liqun Xu, Yuan Li, Bo Xiao, Huan Yang
Myasthenia gravis (MG) is a neurological autoimmune disease characterized by fluctuating weakness of certain voluntary muscles. Current treatments for MG are largely directed at suppressing the whole immune system by using immunosuppressants or glucocorticoids and often cause several side effects. The ideal therapeutic methods for MG should suppress aberrant immunoactivation specifically, while retaining normal function of the immune system. In this study, we first produced exosomes from microRNA-146a overexpressing dendritic cells (DCs)...
August 2017: Inflammation
https://www.readbyqxmd.com/read/28375749/immunization-with-recombinantly-expressed-lrp4-induces-experimental-autoimmune-myasthenia-gravis-in-c57bl-6-mice
#20
Canan Ulusoy, Filiz Çavuş, Vuslat Yılmaz, Erdem Tüzün
BACKGROUND: Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction (NMJ), characterized with muscle weakness. While MG develops due to acetylcholine receptor (AChR) antibodies in most patients, antibodies to muscle-specific receptor tyrosine kinase (MuSK) or low-density lipoprotein receptor-related protein 4 (LRP4) may also be identified. Experimental autoimmune myasthenia gravis (EAMG) has been previously induced by both LRP4 immunization and passive transfer of LRP4 antibodies...
July 2017: Immunological Investigations
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