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Emerging Therapies for the Treatment of Autoimmune Myasthenia Gravis

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Clinical Applications of Immunomics

Part of the book series: Immunomics Reviews ((IMMUN,volume 2))

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Abstract

Myasthenia gravis (MG) is an autoimmune disease mediated by autoantibodies that mainly target muscle nicotinic acetylcholine receptor (AChR) and cause loss of functional AChRs in the neuromuscular junction. Despite extensive knowledge from studies on MG and its major autoantigen, the aetiology of the disease remains unclear, thus rendering therapeutic options unable to target the causative agent. Latest progress on recombinant expression of the AChR subunits has allowed for some alternative, though promising, therapeutic approaches. The scope of this chapter is to provide an overview of the recent achievements in the field of emerging therapeutics for MG, including antigen-specific therapies, which are directed at the autoimmune response.

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Abbreviations

APCs:

antigen-presenting cells

APL:

altered peptide ligand

AChR:

nicotinic acetylcholine receptor

DFP:

double filtration plasmapheresis

EAMG:

experimental autoimmune MG

ECDs:

extracellular domains

EOMG:

early-onset MG

IA:

immunoadsorption

IVIg:

intravenous immunoglobulin

LNCs:

lymph node cells

MIR:

main immunogenic region

mAb:

monoclonal antibody

MG:

myasthenia gravis

MHC:

major histocompatibility complex

MuSK:

muscle-specific kinase

NMJ:

neuromuscular junction

PDEs:

phosphodiesterases

PE:

plasma exchange (plasmapheresis)

TCR:

T cell receptor.

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Acknowledgments

Work in the authors’ laboratories is supported by grants from the QoL program of the European Commission, the Muscular Dystrophy Association (MDA), the Association Française contre les Myopathies (AFM) and the Greek General Secretariat of Research and Technology (GSRT).

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Kostelidou, K., Sideri, A., Lazaridis, K., Fostieri, E., Tzartos, S.J. (2009). Emerging Therapies for the Treatment of Autoimmune Myasthenia Gravis. In: Falus, A. (eds) Clinical Applications of Immunomics. Immunomics Reviews, vol 2. Springer, New York, NY. https://doi.org/10.1007/978-0-387-79208-8_9

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