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Central and peripheral RAG protein re-expression: underestimate mechanisms of tolerance?Hillion S; Rochas C; Devauchelle V; Youinou P; Jamin CScand J Immunol 2006[Sep]; 64 (3): 185-9The generation of developing B cells in the bone marrow is regulated by recombination activating genes RAG1 and RAG2 proteins. They contribute to the synthesis of functional antibodies (Abs) that can present self-reactivities following V(D)J (V, variable; D, diversity and J, joining) recombination. The emergence of autoreactive B cells is prevented by deletion through apoptosis, by stimulation blockade through anergy, or by synthesis of a new B-cell receptor through receptor edition. In the periphery, somatic hypermutation during the course of germinal centre (GC) responses can lead to the appearance of autoreactive and low-affinity Ab-producing B cells. Apoptotic deletion and receptor revision regulate these autoreactive and inappropriate B cells. Moreover, the presence of RAG-positive B cells outside GCs suggest that still uncharacterized regulation checkpoint, associated with secondary V(D)J recombination, also contribute to the regulation of autoreactivities. Failure in central and/or peripheral tolerance mechanisms associated with RAG expression could contribute to the terminal differentiation of autoreactive B cells leading to autoimmune states.|*Immune Tolerance[MESH]|Animals[MESH]|Autoimmunity[MESH]|B-Lymphocytes/immunology/metabolism[MESH]|Bone Marrow/metabolism[MESH]|DNA-Binding Proteins/*metabolism[MESH]|Germinal Center/physiology[MESH]|Homeodomain Proteins/*metabolism[MESH]|Humans[MESH]|Mice[MESH]|Models, Immunological[MESH] |
