{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:06:54Z","timestamp":1786133214911,"version":"build-2736575974"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","funder":[{"DOI":"10.13039\/501100001809","name":"Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81870486"],"award-info":[{"award-number":["81870486"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81870482"],"award-info":[{"award-number":["81870482"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Australian National Health and Medical Research Council Project","award":["1008849"],"award-info":[{"award-number":["1008849"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      Antiglomerular basement membrane (anti-GBM) disease is associated with HLA-DRB1*1501 (the major predisposing genetic factor in the disease), with\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      as a nephritogenic T and B cell epitope. Association of infections with anti-GBM disease has been long suspected. In this study, the authors used bioinformatic tools to search for peptides from microbes mimicking the critical motif of a pathogenic epitope for Goodpasture disease (\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      ). They identified a pathogenic peptide derived from\n                      <jats:italic toggle=\"yes\">Actinomyces<\/jats:italic>\n                      , which was recognized by sera from patients with anti-GBM disease and that induced proteinuria, linear IgG deposition on GBM, and crescent formation in both WKY rats and humanized HLA-DR15 transgenic mice\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      crossreactivity of lymphocytes. These findings implicate a role for infection and molecular mimicry in the pathogenesis of anti-GBM disease.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Antiglomerular basement membrane (anti-GBM) disease is associated with HLA-DRB1*1501 (the major predisposing genetic factor in the disease), with\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      as a nephritogenic T and B cell epitope. Although the cause of disease remains unclear, the association of infections with anti-GBM disease has been long suspected.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To investigate whether microbes might activate autoreactive T and B lymphocytes\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      molecular mimicry in anti-GBM disease, we used bioinformatic tools, including BLAST, SYFPEITHI, and ABCpred, for peptide searching and epitope prediction. We used sera from patients with anti-GBM disease to assess peptides recognized by antibodies, and immunized WKY rats and a humanized mouse model (HLA-DR15 transgenic mice) with each of the peptide candidates to assess pathogenicity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      On the basis of the critical motif, the bioinformatic approach identified 36 microbial peptides that mimic human\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      . Circulating antibodies in sera from patients with anti-GBM recognized nine of them. One peptide, B7, derived from\n                      <jats:italic toggle=\"yes\">Actinomyces<\/jats:italic>\n                      species, induced proteinuria, linear IgG deposition on the GBM, and crescent formation when injected into WKY rats. The antibodies to B7 also targeted human and rat\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      . B7 induced T cell activation from human\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>127\u2013148<\/jats:sub>\n                      -immunized rats. T cell responses to B7 were detected in rats immunized by\n                      <jats:italic toggle=\"yes\">Actinomyces<\/jats:italic>\n                      lysate proteins or recombinant proteins. We confirmed B7\u2019s pathogenicity in HLA-DR15 transgenic mice that developed kidney injury similar to that observed in\n                      <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      3\n                      <jats:sub>135\u2013145<\/jats:sub>\n                      -immunized mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Sera from patients with anti-GBM disease recognized microbial peptides identified through a bioinformatic approach, and a peptide from\n                      <jats:italic toggle=\"yes\">Actinomyces<\/jats:italic>\n                      induced experimental anti-GBM GN by T and B cell crossreactivity. These studies demonstrate that anti-GBM disease may be initiated by immunization with a microbial peptide.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019060619","type":"journal-article","created":{"date-parts":[[2020,5,22]],"date-time":"2020-05-22T14:30:32Z","timestamp":1590157832000},"page":"1282-1295","source":"Crossref","is-referenced-by-count":13,"title":["Experimental Antiglomerular Basement Membrane GN Induced by a Peptide from Actinomyces"],"prefix":"10.1681","volume":"31","author":[{"given":"Qiu-hua","family":"Gu","sequence":"first","affiliation":[{"name":"Renal Division, Peking University First Hospital, Beijing, PR China"},{"name":"Institute of Nephrology, Peking University, Beijing, PR China"},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, PR China"},{"name":"Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3388-313X","authenticated-orcid":false,"given":"Megan","family":"Huynh","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Monash Medical Centre, Clayton, Victoria, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Shi","sequence":"additional","affiliation":[{"name":"Renal Division, Peking University First Hospital, Beijing, PR China"},{"name":"Institute of Nephrology, Peking University, Beijing, PR China"},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, PR China"},{"name":"Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao-yu","family":"Jia","sequence":"additional","affiliation":[{"name":"Renal Division, Peking University First Hospital, Beijing, PR China"},{"name":"Institute of Nephrology, Peking University, Beijing, PR China"},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, PR China"},{"name":"Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie-jian","family":"Luo","sequence":"additional","affiliation":[{"name":"Key Laboratory of Protein and Peptide Pharmaceuticals, National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tai-jiao","family":"Jiang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Protein and Peptide Pharmaceuticals, National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, PR China"},{"name":"Suzhou Institute of Systems Medicine, Suzhou, Jiangsu, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhao","family":"Cui","sequence":"additional","affiliation":[{"name":"Renal Division, Peking University First Hospital, Beijing, PR China"},{"name":"Institute of Nephrology, Peking University, Beijing, PR China"},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, PR China"},{"name":"Key Laboratory of CKD Prevention and Treatment, Ministry of Education of China, Beijing, PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua D.","family":"Ooi","sequence":"additional","affiliation":[{"name":"Centre for Inflammatory Diseases, Department of Medicine, Monash University, Monash Medical Centre, Clayton, Victoria, Australia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2713-2391","authenticated-orcid":false,"given":"A. 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