Identification of Rare Membrane Antigen Specific Human B Cells
DOI:
https://doi.org/10.17161/rrnmf.v4i3.19523Keywords:
autoantibodies, complement, B cells, MACACS, EBV, hybridoma, somatic hypermutationAbstract
The experimentally well supported model that MG pathology is caused by antibodies of the IgG class that bind to AChR at the neuromuscular junction, activate complement, and possibly cause internalization of receptors or their functional blockade has enabled the development of a range of reasonably effective treatments. A better understanding of which B cells are responsible for producing these pathogenic antibodies, and why such B cells develop would enable the development of more targeted therapies. Studies of antibodies isolated from single B cells from patients have provided some of this information that was not available from studies of polyclonal antibodies in sera, but perhaps future studies of the B cells themselves will provide deeper insight into the causes of the disease and thereby enable its prevention.
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