{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T16:41:12Z","timestamp":1791218472393,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,4,7]],"date-time":"2017-04-07T00:00:00Z","timestamp":1491523200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000960","name":"American College of Rheumatology Research and Education Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000960","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["P41 GM104603"],"award-info":[{"award-number":["P41 GM104603"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["S10 OD010724"],"award-info":[{"award-number":["S10 OD010724"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["S10 RR020946"],"award-info":[{"award-number":["S10 RR020946"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatology"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p><jats:italic>Prevotella copri<\/jats:italic>, an intestinal microbe, may overexpand in stool samples from patients with new\u2010onset rheumatoid arthritis (RA), but it is not yet clear whether the organism has immune relevance in RA pathogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>HLA\u2013DR\u2013presented peptides (T cell epitopes) from <jats:italic>P copri<\/jats:italic> were sought directly in the patients' synovial tissue or peripheral blood mononuclear cell (PBMC) samples using tandem mass spectrometry. The antigenicity of peptides or their source proteins was examined in samples from the RA patients or comparison groups. T cell reactivity was determined by enzyme\u2010linked immunospot assay; antibody responses were measured by enzyme\u2010linked immunosorbent assay, and cytokine\/chemokine determinations were made by bead\u2010based assays. Serum and synovial fluid samples were examined for 16S ribosomal DNA for <jats:italic>P copri<\/jats:italic> using nested polymerase chain reaction analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In PBMCs, we identified an HLA\u2013DR\u2013presented peptide from a 27\u2010kd protein of <jats:italic>P copri<\/jats:italic> (<jats:italic>Pc<\/jats:italic>\u2010p27), which stimulated Th1 responses in 42% of patients with new\u2010onset RA. In both new\u2010onset RA patients and chronic RA patients, 1 subgroup had IgA antibody responses to either <jats:italic>Pc<\/jats:italic>\u2010p27 or the whole organism, which correlated with Th17 cytokine responses and frequent anti\u2013citrullinated protein antibodies (ACPAs). The other subgroup had IgG <jats:italic>P copri<\/jats:italic> antibodies, which were associated with <jats:italic>Prevotella<\/jats:italic> DNA in synovial fluid, <jats:italic>P copri<\/jats:italic>\u2013specific Th1 responses, and less frequent ACPAs. In contrast, <jats:italic>P copri<\/jats:italic> antibody responses were rarely found in patients with other rheumatic diseases or in healthy controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Subgroups of RA patients have differential IgG or IgA immune reactivity with <jats:italic>P copri<\/jats:italic>, which appears to be specific for this disease. These observations provide evidence that <jats:italic>P copri<\/jats:italic> is immune\u2010relevant in RA pathogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.40003","type":"journal-article","created":{"date-parts":[[2016,11,18]],"date-time":"2016-11-18T15:36:44Z","timestamp":1479483404000},"page":"964-975","source":"Crossref","is-referenced-by-count":385,"title":["Evidence of the Immune Relevance of <i>Prevotella copri<\/i>, a Gut Microbe, in Patients With Rheumatoid Arthritis"],"prefix":"10.1002","volume":"69","author":[{"given":"Annalisa","family":"Pianta","sequence":"first","affiliation":[{"name":"Massachusetts General Hospital and, Harvard Medical School Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheila","family":"Arvikar","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital and, Harvard Medical School Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klemen","family":"Strle","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital and, Harvard Medical School Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elise E.","family":"Drouin","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital and, Harvard Medical School Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Wang","sequence":"additional","affiliation":[{"name":"Boston University School of Medicine Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine E.","family":"Costello","sequence":"additional","affiliation":[{"name":"Boston University School of Medicine Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen 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