Myasthenia gravis: selective enrichment of antiacetylcholine receptor antibody production in untransformed human B cell cultures

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Item Type:	Article
Title:	Myasthenia gravis: selective enrichment of antiacetylcholine receptor antibody production in untransformed human B cell cultures
Creators Name:	Padberg, F., Matsuda, M., Fenk, R., Patenge, N., Kubuschok, B., Hohlfeld, R., Wekerle, H. and Spuler, S.
Abstract:	B cells producing antibodies against the acetylcholine receptor (AchR) play a central role in the pathogenesis of myasthenia gravis (MG). Although anti-AchR autoantibodies have been studied extensively, not much is known about autoimmune B cells and their antigen-driven activation. This has mainly been due to difficulties in establishing and maintaining untransformed antigen-specific B cells in vitro. In this study, we show that highly enriched B cells from peripheral blood and thymus of MG patients can be maintained in culture over a period of 4 weeks when grown on the AchR-expressing rhabdomyosarcoma cell line TE671 together with an anti-CD40 stimulus and lymphokines. Anti-AchR antibody secretion could be detected in the majority of B cell cultures on TE671 cells up to 4 weeks. In contrast, B cells cultured on CDw32-transfected L cells binding anti-CD40 antibodies (the CD40 system) produced only small amounts of anti-AchR antibodies at single time points, whereas the overall IgG production was higher than on TE671 cells. The expression of the relevant autoantigen on the adherent cell line in addition to other growth stimuli could account for this difference and may provide a useful tool for investigating antigen-dependent B cell activation in MG and other B cell-mediated autoimmune conditions.
Keywords:	CD40, IL-4, IL-10, TE671, Animals, Mice
Source:	European Journal of Immunology
ISSN:	0014-2980
Publisher:	Wiley
Volume:	29
Number:	11
Page Range:	3538-3548
Date:	November 1999
Official Publication:	https://doi.org/10.1002/(SICI)1521-4141(199911)29:11<3538::AID-IMMU3538>3.0.CO;2-Y
PubMed:	View item in PubMed

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