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Acute primary immune responses tend to focus on few immunodominant determinants using a very limitednumber of T cell clones for expansion,whereas chronic inflammatory responses generally recruit a large number ofdifferent T cell clones to attack a broader range of determinants of the invading pathogens or the inflamed tissues.In T cell-mediated organ-specific antoimmune disease,a transition from the acute to the chronic phase contributesto pathogenesis,and the broadening process is called determinant spreading.The cellular components catalyzingthe spreading reaction are not identified.It has been suggested that autoreactive B cells may play a central role indiversifying autoreactive T cell responses,possibly through affecting antigen processing and presentation.Theclonal identity and diversity of the B cells and antibodies seem critical in regulating T cell activity and subsequenttissue damage or repair.Here,we use two autoimmune animal models,experimental autoimmune thyroiditis(EAT)and type 1 diabetes(T1D),to discuss how autoreactive B cells or antibodies alter the processing and presentation ofautoantigens to regulate specific T cell response.Cellular & Molecular Immunology.2005;2(3):169-175.
Acute primary immune responses tend to focus on few immunodominant determinants using a very limited number of T cell clones for expansion, of chronic inflammatory responses generally recruit a large number of different T cell clones to attack a broader range of determinants of the invading pathogens or the inflamed tissues In T cell-mediated organ-specific antoimmune disease, a transition from the acute to the chronic phase contributesto pathogenesis, and the broadening process is determinant spreading. The cellular components catalyzing the spreading reaction are not identified. It has been suggested that autoreactive B cells may play a central role indiversifying autoreactive T cell responses, possibly through affecting antigen processing and presentation. Theonal identity and diversity of the B cells and antibodies seem critical in regulating T cell activity and subsequent damage damage or repair. Here, we use two autoimmune animal models, experimental autoimmune thyroiditis (EAT) an d type 1 diabetes (T1D), to discuss how autoreactive B cells or antibodies alter the processing and presentation of autoantigens to regulate specific T cell response. Cellular & Molecular Immunology. 2005; 2 (3): 169-175.