Journal
IMMUNITY
Volume 15, Issue 6, Pages 947-957Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(01)00251-5
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Receptor editing is a means by which immature bone marrow B cells can become self-tolerant. Rearrangements of heavy (H) and/or light (L) chain genes are induced by encounter with autoantigens to change the specificity from self to nonself. We have developed site-directed transgenic mice (sd-tg) whose transgenes code for the H chain of antibodies that bind DNA. B cells that express the transgenic H chain associate mainly with four of the 93 functional VK genes of the mouse. Numerous aspartate residues that might inhibit DNA binding by the VH domain distinguish these L chain VK sequences, but engaging these VK editors often requires multiple rearrangements. Among the edited B cells is a subset of multispecific cells that express multiple receptors. One consequence of multispecificity is partial autoreactivity; these multispecific B cells may contribute to autoimmunity.
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