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Autoantibodies make a U-turn: the toll hypothesis for autoantibody specificity Martin DA; Elkon KBJ Exp Med 2005[Dec]; 202 (11): 1465-9Like the immune response itself, our efforts to understand the "rules" for self-nonself discrimination are constantly evolving. The discovery of pattern recognition receptors-the Toll-like receptor (TLR) family in particular-shifted the emphasis of self-nonself recognition from lymphocytes functioning in the adaptive immune system to antigen-presenting cells (APCs) functioning in the innate immune system. Two new articles, one in a recent issue (1) and one in this issue (see Vollmer et al. [2] on p. 1575), demonstrate that antigen-antibody complexes containing RNAs activate B lymphocytes and dendritic cells (DCs) through interaction with TLR7 and/or TLR8. From these and other papers, one begins to see how specific types of autoantigens-by virtue of their capacity to act as TLR ligands-favor autoantibody production. This is known as the Toll hypothesis.|Animals[MESH]|Antibody Formation/immunology[MESH]|Autoantibodies/immunology[MESH]|Autoimmune Diseases/*immunology[MESH]|B-Lymphocytes/*immunology[MESH]|Dendritic Cells[MESH]|Humans[MESH]|RNA/*immunology[MESH]|Self Tolerance/*immunology[MESH]|Signal Transduction/immunology[MESH]|Toll-Like Receptor 7/*immunology[MESH]|Toll-Like Receptor 8/*immunology[MESH] |
