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Circulating memory B cells are reduced in patients with late‐onset myasthenia gravis
Author(s) -
Kubota Akihiro,
Izaki Shoko,
Fukaura Hikoaki,
Nomura Kyoichi
Publication year - 2015
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12203
Subject(s) - myasthenia gravis , lymphocyte , immunology , autoantibody , group b , group a , memory b cell , medicine , b cell , antibody
Objective Myasthenia gravis ( MG ) is an autoimmune disorder of unknown cause where neural transmission is blocked at the neuromuscular junction. Although it has been shown that patients with MG show various differences in clinical characteristics depending on the age of onset, differences in pathology remain unclear. Methods In the present study, we divided patients with MG into a late‐onset group ( n = 26) and an early‐onset group ( n = 29), and measured T and B lymphocyte subsets using surface markers. Results When T lymphocyte subsets and B lymphocyte subsets (transitional B cells, naïve B cells, memory B cells and plasmablasts) were examined, it was found that the percentage of memory B cells was significantly lower in the late‐onset group relative to age‐matched healthy controls. However, no significant difference was seen between the early‐onset group and healthy controls. When the percentage of memory B cells was compared between the late‐onset group and the early‐onset group, it was found to be significantly lower in the late‐onset group. A decrease in circulating memory B cells in patients with late‐onset MG was also seen when circulating memory B cells were activated, and proceeded to penetrate and embed in tissue in the lymph nodes and the thymus. It appears that memory B cells that have penetrated and embedded in tissue begin producing autoantibodies after they differentiate from plasmablasts into plasma cells. Conclusions A reduced percentage of memory B cells appears to be a characteristic of late‐onset MG observed in circulating T and B lymphocyte subsets.