Autoreactive B cells get activated in extrafollicular sites.
Autoreactive B cells are prevented from producing autoantibodies that may cause pathogenicity in autoimmune diseases by the induction of tolerance. When autoreactive B cells escape regulation in autoimmune-prone individuals, large amounts of autoantibodies are produced with somatic mutations in their variable regions. In this issue of the European Journal of Immunology, a new and very useful model is presented that induces activation and hypermutation of autoreactive B cells upon injection of chromatin-containing immune complexes. The differentiation and hypermutation of autoreactive B cells takes place at extrafollicular sites.
Hematopoiesis Unit, Institute for Biology, Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nuremberg, Germany.
Florian
F
Weisel
Ute
U
Wellmann
Thomas H
TH
Winkler
D000818:Animals; D015551:Autoimmunity / Q000276:immunology*; D016175:B-Lymphocyte Subsets / Q000276:immunology*; D002843:Chromatin / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D051379:Mice; D008807:Mice, Inbred BALB C; D019463:Mice, Inbred MRL lpr / Q000276:immunology; D008822:Mice, Transgenic; D009707:Nucleosomes / Q000276:immunology; D009928:Organ Specificity; D010316:Particle Size; D012217:Rheumatoid Factor / Q000276:immunology; D027041:Somatic Hypermutation, Immunoglobulin; D013154:Spleen / Q000276:immunology* / Q000648:ultrastructure; D051193:Toll-Like Receptors / Q000276:immunology
D002843:Chromatin; D007074:Immunoglobulin G; D009707:Nucleosomes; D051193:Toll-Like Receptors; D012217:Rheumatoid Factor