B cell receptor editing in tolerance and autoimmunity.
The random assembly of immunoglobulin (Ig) genes often creates a B cell receptor that is self-reactive, and such cells are subjected to negative selection. A primary mechanism to extinguish this self-reactivity is receptor editing, which allows continued recombination of Ig genes and replacement of the self-reactive receptor with a new innocuous receptor. Recent data now suggest that receptor editing may also promote autoimmunity in an autoimmune context. This mechanism has also been implicated in the process of B cell positive selection and maturation. Here we discuss the contribution of receptor editing in B-lymphopoiesis and its importance for B cell tolerance and autoimmunity.
Azulay-Debby
Hilla
H
Department of Immunology, Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel.
Melamed
Doron
D
D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology*; D015326:Gene Rearrangement, B-Lymphocyte, Heavy Chain; D015328:Gene Rearrangement, B-Lymphocyte, Light Chain; D006801:Humans; D038041:Lymphopoiesis; D011947:Receptors, Antigen, B-Cell / Q000235:genetics; D017634:Self Tolerance
D011947:Receptors, Antigen, B-Cell