Autoantibodies from Synovial Lesions in Chronic, Antibiotic Treatment-Resistant Lyme Arthritis Bind Cytokeratin-10 Export

@article{citeulike:784955, abstract = {Although the causative agent of Lyme disease is definitively known to be the tick-borne spirochete, Borrelia burgdorferi, the etiology of chronic joint inflammation that ensues in a subset of patients remains less well understood. Persistence of arthritis after apparent eradication of the spirochete suggests an autoimmune reaction downstream of the original bacterial infection. We have generated recombinant Ab probes from synovial lesions within affected arthritic joints in an attempt to recapitulate disease-relevant Ag-binding specificities at the site of injury. Using this panel of intra-articular probes, as well as Ab fragments derived from patient peripheral blood, we have identified cytokeratin 10, present in synovial microvascular endothelium, as a target ligand and a putative autoantigen in chronic, antibiotic treatment-resistant Lyme arthritis. Furthermore, there is cross-reactivity between cytokeratin 10 and a prominent B. burgdorferi Ag, outer surface protein A. Release of the self protein in the context of inflammation-induced tissue injury and the resulting in situ response to it could set in motion a feed-forward loop, which amplifies the inflammatory process, thereby rendering it chronic and self-perpetuating, even in the absence of the inciting pathogen.}, author = {Ghosh, Srimoyee and Seward, Robert and Costello, Catherine E. and Stollar, David B. and Huber, Brigitte T.}, citeulike-article-id = {784955}, citeulike-linkout-0 = {http://www.jimmunol.org/cgi/content/abstract/177/4/2486}, day = {15}, journal = {J Immunol}, keywords = {autoantibodies, bcell, lymedisease, molecularmimicry}, month = {August}, number = {4}, pages = {2486--2494}, posted-at = {2006-08-03 18:44:45}, priority = {2}, title = {Autoantibodies from Synovial Lesions in Chronic, Antibiotic Treatment-Resistant Lyme Arthritis Bind Cytokeratin-10}, url = {http://www.jimmunol.org/cgi/content/abstract/177/4/2486}, volume = {177}, year = {2006} }

TY - JOUR ID - citeulike:784955 L3 - citeulike-article-id:784955 N2 - Although the causative agent of Lyme disease is definitively known to be the tick-borne spirochete, Borrelia burgdorferi, the etiology of chronic joint inflammation that ensues in a subset of patients remains less well understood. Persistence of arthritis after apparent eradication of the spirochete suggests an autoimmune reaction downstream of the original bacterial infection. We have generated recombinant Ab probes from synovial lesions within affected arthritic joints in an attempt to recapitulate disease-relevant Ag-binding specificities at the site of injury. Using this panel of intra-articular probes, as well as Ab fragments derived from patient peripheral blood, we have identified cytokeratin 10, present in synovial microvascular endothelium, as a target ligand and a putative autoantigen in chronic, antibiotic treatment-resistant Lyme arthritis. Furthermore, there is cross-reactivity between cytokeratin 10 and a prominent B. burgdorferi Ag, outer surface protein A. Release of the self protein in the context of inflammation-induced tissue injury and the resulting in situ response to it could set in motion a feed-forward loop, which amplifies the inflammatory process, thereby rendering it chronic and self-perpetuating, even in the absence of the inciting pathogen. IS - 4 JF - J Immunol EP - 2494 TI - Autoantibodies from Synovial Lesions in Chronic, Antibiotic Treatment-Resistant Lyme Arthritis Bind Cytokeratin-10 VL - 177 SP - 2486 KW - autoantibodies KW - bcell KW - lymedisease KW - molecularmimicry AU - Ghosh, Srimoyee AU - Seward, Robert AU - Costello, Catherine AU - Stollar, David AU - Huber, Brigitte PY - 2006/08/15/ UR - http://www.jimmunol.org/cgi/content/abstract/177/4/2486 ER -