B cells in the pathophysiology of myasthenia gravis.

Published

Journal Article (Review)

Myasthenia gravis (MG) is an archetypal autoimmune disease. The pathology is characterized by autoantibodies to the acetylcholine receptor (AChR) in most patients or to muscle-specific tyrosine kinase (MuSK) in others and to a growing number of other postsynaptic proteins in smaller subsets. A decrease in the number of functional AChRs or functional interruption of the AChR within the muscle end plate of the neuromuscular junction is caused by pathogenic autoantibodies. Although the molecular immunology underpinning the pathology is well understood, much remains to be learned about the cellular immunology contributing to the production of autoantibodies. This Review documents research concerning the immunopathology of MG, bringing together evidence principally from human studies with an emphasis on the role of adaptive immunity and B cells in particular. Proposed mechanisms for autoimmunity, which take into account that different types of MG may incorporate divergent immunopathology, are offered. Muscle Nerve 57: 172-184, 2018.

Full Text

Duke Authors

Cited Authors

  • Yi, JS; Guptill, JT; Stathopoulos, P; Nowak, RJ; O'Connor, KC

Published Date

  • February 2018

Published In

Volume / Issue

  • 57 / 2

Start / End Page

  • 172 - 184

PubMed ID

  • 28940642

Pubmed Central ID

  • 28940642

Electronic International Standard Serial Number (EISSN)

  • 1097-4598

Digital Object Identifier (DOI)

  • 10.1002/mus.25973

Language

  • eng

Conference Location

  • United States