{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T19:58:56Z","timestamp":1770839936345,"version":"3.50.1"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2024,3,13]],"date-time":"2024-03-13T00:00:00Z","timestamp":1710288000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,3,13]],"date-time":"2024-03-13T00:00:00Z","timestamp":1710288000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"HHS | National Institutes of Health","award":["F31AI161962"],"award-info":[{"award-number":["F31AI161962"]}]},{"name":"HHS | National Institutes of Health","award":["U01AI160664"],"award-info":[{"award-number":["U01AI160664"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2024,3,13]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:sec>\n            <jats:title\/>\n            <jats:p>\n              Mice that lack the genes for IL-27, or the IL-27 receptor, and infected with\n              <jats:italic>Toxoplasma gondii<\/jats:italic>\n              develop T cell-mediated pathology. Here, studies were performed to determine the impact of endogenous IL-27 on the immune response to\n              <jats:italic>T. gondii<\/jats:italic>\n              in wild-type (WT) mice. Analysis of infected mice revealed the early production of IL-27p28 by a subset of Ly6C\n              <jats:sup>hi<\/jats:sup>\n              , inflammatory monocytes, and sustained IL-27p28 production at sites of acute and chronic infection. Administration of anti-IL-27p28 prior to infection resulted in an early (day 5) increase in levels of macrophage and granulocyte activation, as well as enhanced effector T cell responses, as measured by both cellularity, cytokine production, and transcriptional profiling. This enhanced acute response led to immune pathology, while blockade during the chronic phase of infection resulted in enhanced T cell responses but no systemic pathology. In the absence of IL-27, the enhanced monocyte responses observed at day 10 were a secondary consequence of activated CD4\n              <jats:sup>+<\/jats:sup>\n              T cells. Thus, in WT mice, IL-27 has distinct suppressive effects that impact innate and adaptive immunity during different phases of this infection.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              The molecule IL-27 is critical in limiting the immune response to the parasite\n              <jats:italic>Toxoplasma gondii<\/jats:italic>\n              . In the absence of IL-27, a lethal, overactive immune response develops during infection. However, when exactly in the course of infection this molecule is needed was unclear. By selectively inhibiting IL-27 during this parasitic infection, we discovered that IL-27 was only needed during, but not prior to, infection. Additionally, IL-27 is only needed in the active areas in which the parasite is replicating. Finally, our work found that a previously unstudied cell type, monocytes, was regulated by IL-27, which contributes further to our understanding of the regulatory networks established by this molecule.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.00083-24","type":"journal-article","created":{"date-parts":[[2024,2,20]],"date-time":"2024-02-20T14:01:05Z","timestamp":1708437665000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":14,"title":["Endogenous IL-27 during toxoplasmosis limits early monocyte responses and their inflammatory activation by pathological T cells"],"prefix":"10.1128","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2224-5159","authenticated-orcid":true,"given":"Daniel L.","family":"Aldridge","sequence":"first","affiliation":[{"name":"University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Devapregasan","family":"Moodley","sequence":"additional","affiliation":[{"name":"Abata Therapeutics, Waltham, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0340-9181","authenticated-orcid":true,"given":"Jeongho","family":"Park","sequence":"additional","affiliation":[{"name":"University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA"},{"name":"Kangwon National University College of Veterinary Medicine and Institute of Veterinary Science, Chuncheon, South Korea"},{"name":"Multidimensional Genomics Research Center, Kangwon National University, Chuncheon, South Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anthony T.","family":"Phan","sequence":"additional","affiliation":[{"name":"University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew","family":"Rausch","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kerry F.","family":"White","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yue","family":"Ren","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karin","family":"Golin","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Enrico","family":"Radaelli","sequence":"additional","affiliation":[{"name":"Comparative Pathology Core, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ross","family":"Kedl","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"},{"name":"University of Colorado, Anschuitz Medical Campus, Aurora, Colorado, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pamela M.","family":"Holland","sequence":"additional","affiliation":[{"name":"InduPro, Seattle, Washington, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan","family":"Hill","sequence":"additional","affiliation":[{"name":"Surface Oncology, Cambridge, Massachusetts, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3092-1428","authenticated-orcid":true,"given":"Christopher A.","family":"Hunter","sequence":"additional","affiliation":[{"name":"University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, 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