Immunoadsorption apheresis versus intravenous immunoglobulin therapy for exacerbation of myasthenia gravis

2021 ◽  
Author(s):  
Manato Yasuda ◽  
Akiyuki Uzawa ◽  
Yukiko Ozawa ◽  
Yuta Kojima ◽  
Yosuke Onishi ◽  
...  
Keyword(s):  
Myasthenia Gravis ◽  
Intravenous Immunoglobulin ◽  
Immunoglobulin Therapy ◽  
Intravenous Immunoglobulin Therapy

High-dose intravenous immunoglobulin therapy for myasthenia gravis

1997 ◽  
Vol 245 (1) ◽  
pp. 26-31 ◽  
Author(s):  
J. L. M. Jongen ◽  
P. A. van Doorn ◽  
Frans G. A. van der Meché
Keyword(s):  
Myasthenia Gravis ◽  
Intravenous Immunoglobulin ◽  
Immunoglobulin Therapy ◽  
High Dose ◽  
Intravenous Immunoglobulin Therapy

scholarly journals Defects of CTLA-4 Are Associated with Regulatory T Cells in Myasthenia Gravis Implicated by Intravenous Immunoglobulin Therapy

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Wenhua Xu ◽  
Mingshan Ren ◽  
Swagata Ghosh ◽  
Kai Qian ◽  
Zhaofeng Luo ◽  
...  
Keyword(s):  
T Cells ◽  
Myasthenia Gravis ◽  
Intravenous Immunoglobulin ◽  
Ivig Therapy ◽  
Immunoglobulin Therapy ◽  
Treg Cells ◽  
Ivig Treatment ◽  
Intravenous Immunoglobulin Therapy ◽  
Circulating Autoantibodies ◽  
Antigen Presenting

Myasthenia gravis (MG) is a CD4+ T cell-dependent autoimmune disease resulting from aberrant immune response mediated by circulating autoantibodies at the neuromuscular junction. Intravenous immunoglobulin (IVIg) is an expensive and commonly used immunotherapeutic approach to treat patients with MG. The mechanisms of actions involved in IVIg treatment, however, remain to be investigated. In an effort to examine the roles of various subsets of CD4+ T cells in the periphery blood of MG and uncover the mechanisms that contribute to the therapeutical effects of IVIg, we first demonstrated that a subset of CD4+ T cells, CTLA-4-expressing regulatory T (Treg) cells, were underrepresented and functionally defective in MG patients. The dynamic profiling during the IVIg therapy course further revealed an inverse relationship between the frequency of CTLA-4+ Treg and the quantitative MG (QMG) score that represents disease severity. Our mechanistic studies indicated that IVIg expands CTLA-4-Treg cells via modulating antigen-presenting dendritic cells (DCs). To determine the molecular defects of CTLA-4 in abnormities of Treg in MG patients, we demonstrated hypermethylation at -658 and -793 CpGs of CTLA-4 promoter in MG Tregs. Interestingly, IVIg therapy significantly reduced the methylation level at these two sites in MG patients. Overall, our study may suggest a role of CTLA-4 in functionally defected Treg cells in MG and its actions involved in IVIg therapy.

scholarly journals Escalation Strategies in the Treatment of Refractory Myasthenia Gravis

2018 ◽  
Vol 02 (01) ◽  
pp. E56-E59
Author(s):  
Sarah Hoffmann ◽  
Andreas Meisel
Keyword(s):  
Myasthenia Gravis ◽  
Intravenous Immunoglobulin ◽  
Immunoglobulin Therapy ◽  
Consensus Guidelines ◽  
International Consensus ◽  
Intravenous Immunoglobulin Therapy ◽  
International Consensus Guidelines

AbstractAmong all patients with myasthenia gravis (MG), 10 to 15% are considered to be refractory to (expanded) standard treatments. Current international consensus guidelines for the management of myasthenia gravis recommend referral of refractory MG patients to centers with expertise in the treatment of MG and chronic intravenous immunoglobulin therapy or plasmapheresis. Here we briefly summarize current approaches to overcome refractory myasthenia gravis.

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