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• W2016049846 abstract "CD22-deficient mice are characterized by B cell hyperactivity and autoimmunity. We have constructed knock-in CD22-/- mice, expressing an anti-DNA heavy (H) chain (D42), alone or combined with Vkappa1-Jkappa1 or Vkappa8-Jkappa5 light (L) chains. The Ig-targeted mice produced a lupus-like serology that was age- and sex-dependent. High-affinity IgG autoantibodies were largely dependent on the selection of B cells with a particular H/L combination, in which a non-transgenic, endogenous L chain was assembled by secondary rearrangements through the mechanism of receptor editing. Moreover, we present evidence that these secondary rearrangements are very prominent in splenic peripheral B cells. Since CD22 is primarily expressed on the surface of peripheral B cells, we propose a model for the development of a lupus-like autoimmune disease by a combination of peripheral receptor editing and abnormal B cell activation." @default.
• W2016049846 created "2016-06-24" @default.
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• W2016049846 date "2006-10-01" @default.
• W2016049846 modified "2023-09-26" @default.
• W2016049846 title "Peripheral B cell receptor editing may promote the production of high-affinity autoantibodies in CD22-deficient mice" @default.
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• W2016049846 doi "https://doi.org/10.1002/eji.200636190" @default.
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