{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T02:36:22Z","timestamp":1772678182875,"version":"3.50.1"},"reference-count":76,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2025,1,6]],"date-time":"2025-01-06T00:00:00Z","timestamp":1736121600000},"content-version":"vor","delay-in-days":2562,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>CD40\/CD40L interactions play a critical role in immunity and autoimmunity. In this study, we sought to understand the requirement for CD40 signaling in the programmed cell death-1 (PD-1) checkpoint and CD28 costimulatory pathways important for maintenance of peripheral tolerance. Blocking either pathway can result in loss of self-tolerance and development of autoimmunity. We found that primary Sj\u00f6gren\u2019s syndrome (pSS) and autoimmune thyroid diseases (ATDs) that develop spontaneously in CD28-deficient IFN-\u03b3\u2212\/\u2212 NOD.H-2h4 (CD28\u2212\/\u2212) mice required CD40 signaling. Specifically, blockade of CD40L with the anti-CD40L mAb, MR1, inhibited autoantibody production and inflammation in thyroid and salivary gland target tissues. Unexpectedly, however, ATD and pSS in PD-1\u2013deficient IFN-\u03b3\u2212\/\u2212 NOD.H-2h4 (PD-1\u2212\/\u2212) mice developed independently of CD40\/CD40L interactions. Treatment with MR1 had no effect and even exacerbated disease development in pSS and ATD, respectively. Most interesting, anti-thyroglobulin and pSS-associated autoantibodies were increased following anti-CD40L treatment, even though MR1 effectively inhibited the spontaneous splenic germinal centers that form in PD-1\u2013deficient mice. Importantly, blockade of the PD-1 pathway by administration of anti\u2013PD-1 mAb in CD28\u2212\/\u2212 mice recapitulated the PD-1\u2212\/\u2212 phenotype, significantly impacting the ability of MR1 to suppress ATD and pSS in these mice. These results indicate that there can be different pathways and requirements to autoimmune pathogenesis depending on the availability of specific checkpoint and costimulatory receptors, and an intact PD-1 pathway is apparently required for inhibition of autoimmunity by anti-CD40L.<\/jats:p>","DOI":"10.4049\/immunohorizons.1700069","type":"journal-article","created":{"date-parts":[[2018,1,24]],"date-time":"2018-01-24T01:50:12Z","timestamp":1516758612000},"page":"54-66","source":"Crossref","is-referenced-by-count":17,"title":["Requirement for CD40\/CD40L Interactions for Development of Autoimmunity Differs Depending on Specific Checkpoint and Costimulatory Pathways"],"prefix":"10.1093","volume":"2","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5553-6273","authenticated-orcid":false,"given":"Elisaveta","family":"Voynova","sequence":"first","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Group, Medimmune LLC , Gaithersburg, MD 20878"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tamer","family":"Mahmoud","sequence":"additional","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Group, Medimmune LLC , Gaithersburg, MD 20878"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucas T","family":"Woods","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Christopher S. Bond Life Sciences Center, University of Missouri , Columbia, MO 65211"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3246-6353","authenticated-orcid":false,"given":"Gary A","family":"Weisman","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Christopher S. Bond Life Sciences Center, University of Missouri , Columbia, MO 65211"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3761-9571","authenticated-orcid":false,"given":"Rachel","family":"Ettinger","sequence":"additional","affiliation":[{"name":"Respiratory, Inflammation and Autoimmunity Group, Medimmune LLC , Gaithersburg, MD 20878"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helen","family":"Braley-Mullen","sequence":"additional","affiliation":[{"name":"Department of Medicine and Microbiology, University of Missouri , Columbia, MO 65212"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2018,1,23]]},"reference":[{"key":"2025010608283373700_r1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/bs.ai.2014.11.001","article-title":"NOD.H-2h4 mice: an important and underutilized animal model of autoimmune thyroiditis and Sj\u00f6gren\u2019s syndrome","volume":"126","author":"Braley-Mullen","year":"2015","journal-title":"Adv. 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