Clonal expansions of CD4+ B helper T cells in autoimmune myasthenia gravis

The weakness in myasthenia gravis (MG) is mediated by T helper cell (Th)‐dependent autoantibodies against neuromuscular epitopes. So far, analyzing Th phenotypes or antigen specificities has yielded very few clues to pathogenesis. Here we adopt an alternative antigen‐independent approach, analyzing...

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Bibliographic Details
Published in:European journal of immunology 2007-03, Vol.37 (3), p.849-863
Main Authors: Tackenberg, Björn, Kruth, Jens, Bartholomaeus, Johanna E., Schlegel, Kerstin, Oertel, Wolfgang H., Willcox, Nicholas, Hemmer, Bernhard, Sommer, Norbert
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Aged, 80 and over
Amino Acid Sequence
Autoimmunity
Cell Proliferation
Clone Cells
Female
Genes, T-Cell Receptor beta
Humans
Immunoglobulin Variable Region - biosynthesis
Immunoglobulin Variable Region - genetics
Male
Middle Aged
Molecular Sequence Data
Myasthenia gravis
Myasthenia Gravis - genetics
Myasthenia Gravis - immunology
Oligoclonal
T cell receptor
T-Lymphocytes, Helper-Inducer - immunology
T-Lymphocytes, Helper-Inducer - metabolism
T-Lymphocytes, Helper-Inducer - pathology
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Summary:The weakness in myasthenia gravis (MG) is mediated by T helper cell (Th)‐dependent autoantibodies against neuromuscular epitopes. So far, analyzing Th phenotypes or antigen specificities has yielded very few clues to pathogenesis. Here we adopt an alternative antigen‐independent approach, analyzing T cell receptor (TCR) Vβ usage/expansions in blood from 118 MG patients. We found major expansions (⩾ five standard deviations above the mean of 118 healthy, individually age‐ and sex‐matched controls) in diverse Vβ in 21 patients (17.6%, p
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200636449