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Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity
Published on: April 11, 2019
B cell receptor editing in tolerance and autoimmunity
Hilla Azulay-Debby1, Doron Melamed
1Department of Immunology, Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel.
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.
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.
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