Kristin S, Herrmann M, Winkler T (2013)
Publication Status: Published
Publication Type: Journal article, Review article
Publication year: 2013
Book Volume: 46
Pages Range: 121-127
Journal Issue: 2
DOI: 10.3109/08916934.2012.748751
The formation of antibodies against double-stranded (ds)DNA is considered to be the serologic hallmark of systemic lupus erythematosus (SLE) and anti-dsDNA antibodies play an important role in the pathogenesis of the disease. Anti-dsDNA antibodies from lupus mice and SLE patients arise by somatic mutation. Importantly, autoantibodies in which somatic mutations have been reverted to germ-line V regions did not show any measurable autoreactivity, suggesting that anti-dsDNA autoantibodies develop from non-autoreactive B-cells by somatic hypermutation, presumably during the germinal center reaction. As the random nature of somatic hypermutation will inevitably create autoreactive B cells, self-tolerance checkpoints at the postmutational stage of B cell differentiation have to exist that normally prevent the induction of pathogenic anti-dsDNA specificities. This review summarizes the proposed mechanisms for the generation of anti-dsDNA in murine lupus and in SLE patients. © Informa UK, Ltd.
APA:
Kristin, S., Herrmann, M., & Winkler, T. (2013). The role of somatic hypermutation in the generation of pathogenic antibodies in SLE. Autoimmunity, 46(2), 121-127. https://doi.org/10.3109/08916934.2012.748751
MLA:
Kristin, Schröder, Martin Herrmann, and Thomas Winkler. "The role of somatic hypermutation in the generation of pathogenic antibodies in SLE." Autoimmunity 46.2 (2013): 121-127.
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