{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T22:17:50Z","timestamp":1790720270034,"version":"4.1.0"},"reference-count":217,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T00:00:00Z","timestamp":1767744000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01DE030095\u201001A1"],"award-info":[{"award-number":["1R01DE030095\u201001A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01DK140281\u201001A1"],"award-info":[{"award-number":["1R01DK140281\u201001A1"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Periodontal Research"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Autoimmunity arises when central and peripheral immune tolerance fails, allowing self\u2010reactive T and B cells to attack host tissues. Immune attack on host tissues gives rise to a spectrum of autoimmune diseases. This narrative review explains the basic immune mechanisms that may contribute to systemic autoimmunity and exacerbate periodontitis. Current evidence suggests that during T cell development in the thymus, the risk of overt self\u2010reactivity is reduced by the elimination of thymocytes that recognize self\u2010epitopes with high affinity. Despite this stringent editing, some T cells specific for self\u2010peptides escape deletion and persist as dormant cells in the circulation. Dormant cells can remain functionally inactive or anergic due to insufficient co\u2010stimulatory signals, maintaining peripheral self\u2010tolerance. During infection or tissue injury, neutrophil activation, microbial enzymes, and host peptidyl\u2010arginine deiminases (PADs) can catalyze citrullination of self\u2010proteins, generating structurally altered epitopes (neoantigens). In periodontitis, the neoantigen pool is expanded during NETosis, inflammation\u2010driven post\u2010translational modifications of proteins. Modifications are made collectively by peptidyl\u2010arginine deiminases (PADs) produced by\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    and the host. Hence, dormant autoreactive T cells are activated by antigen\u2010presenting cells (APCs) displaying these modified self\u2010antigens or cross\u2010reactive microbial peptides on MHC molecules in the presence of microbial\u2010 or danger\u2010associated molecular pattern molecules (MAMPs\/DAMPs). Once activated, these autoreactive CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells differentiate into effector cells. These effector T cells can break tolerance, providing cognate help to B cells to promote autoantibody production. Autoreactive B cells arise stochastically during early B cell development through random somatic recombination of immunoglobulin genes. Affinity maturation and epitope spreading broaden the B cell receptor (BCR) repertoire generating autoreactive B cells. Normally restrained, these B cells become activated when their BCRs engage self\u2010antigens in the presence of strong proinflammatory cues (MAMPs\/DAMPs). With cognate help from autoreactive T helper cells, B cells undergo class\u2010switching and sustained autoantibody production. Together, autoreactive T cells and B cell\u2010derived autoantibodies drive cellular and humoral autoimmunity, respectively. Compelling mechanistic and clinical evidence support a model in which periodontal pathobionts like\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>A. actinomycetemcomitans<\/jats:italic>\n                    <\/jats:styled-content>\n                    contribute to systemic autoimmunity via processes including protein citrullination, epitope spreading and molecular mimicry between microbial and host antigens, which further amplify cross\u2010reactivity. These interactions are most clearly illustrated in RA but increasingly implicated in other diseases such as IBD and AD. Thus, periodontitis not only causes local immune\u2010mediated tissue destruction but also facilitates systemic dissemination of autoreactive T and B cells, thereby contributing to the initiation and\/or exacerbation of autoimmune diseases.\n                  <\/jats:p>","DOI":"10.1111\/jre.70058","type":"journal-article","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T12:09:48Z","timestamp":1767787788000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Autoimmunity and Periodontitis"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5922-3709","authenticated-orcid":false,"given":"Massimo","family":"Costalonga","sequence":"first","affiliation":[{"name":"Division of Basic Sciences, Department of Diagnostic and Biological Sciences, School of Dentistry University of Minnesota  Minneapolis Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8279-3766","authenticated-orcid":false,"given":"Vivek","family":"Thumbigere\u2010Math","sequence":"additional","affiliation":[{"name":"Division of Periodontics, Department of Advanced Oral Sciences and Therapeutics, School of Dentistry University of Maryland  Baltimore Maryland USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark C.","family":"Herzberg","sequence":"additional","affiliation":[{"name":"Division of Basic Sciences, Department of Diagnostic and Biological Sciences, School of Dentistry University of Minnesota  Minneapolis Minnesota USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,1,7]]},"reference":[{"issue":"3","key":"e_1_2_17_2_1","doi-asserted-by":"crossref","first-page":"177","DOI":"10.3109\/08916939209004822","article-title":"Assessment of Antibody Dependent Cell Cytotoxicity in Autoimmune Thyroid Disease Using Porcine Thyroid Cells","volume":"13","author":"Rodien P.","year":"1992","journal-title":"Autoimmunity"},{"issue":"11","key":"e_1_2_17_3_1","doi-asserted-by":"crossref","first-page":"6747","DOI":"10.1073\/pnas.1031503100","article-title":"T Lymphoid Differentiation in Human Bone Marrow","volume":"100","author":"Klein F.","year":"2003","journal-title":"Proceedings of the National Academy of Sciences of the United States of America"},{"issue":"6","key":"e_1_2_17_4_1","doi-asserted-by":"crossref","first-page":"377","DOI":"10.1038\/nri3667","article-title":"Positive and Negative Selection of the T Cell Repertoire: What Thymocytes See (And Don't See)","volume":"14","author":"Klein L.","year":"2014","journal-title":"Nature Reviews. 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