[PDF][PDF] Editors and editing of anti-DNA receptors

H Li, Y Jiang, EL Prak, M Radic, M Weigert - Immunity, 2001 - cell.com
H Li, Y Jiang, EL Prak, M Radic, M Weigert
Immunity, 2001cell.com
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 Vκ genes of the mouse. Numerous aspartate residues that might …
Abstract
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 Vκ genes of the mouse. Numerous aspartate residues that might inhibit DNA binding by the VH domain distinguish these L chain Vκ sequences, but engaging these Vκ 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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