{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:06:46Z","timestamp":1791194806615,"version":"4.1.0"},"reference-count":35,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6106","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2012,10,26]]},"abstract":"<jats:title>Treg-ulating Immune Responses<\/jats:title>\n                  <jats:p>\n                    There are many checks and balances to keep the immune system from running amok. One of the most critical is a specialized population of T cells, called regulatory T cells (T\n                    <jats:sub>regs<\/jats:sub>\n                    ). In their absence, a lethal autoimmune disease develops in both humans and mice. Although T\n                    <jats:sub>regs<\/jats:sub>\n                    are well known for their suppression of autoimmune responses, how they modulate responses to infectious agents is less well understood. Using inducible deletion of T\n                    <jats:sub>regs<\/jats:sub>\n                    in mice,\n                    <jats:bold>\n                      Pace\n                      <jats:italic>et al.<\/jats:italic>\n                    <\/jats:bold>\n                    (p.\n                    <jats:related-article xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" page=\"532\" related-article-type=\"in-this-issue\" vol=\"338\" xlink:href=\"10.1126\/science.1227049\">532<\/jats:related-article>\n                    ) showed that T\n                    <jats:sub>regs<\/jats:sub>\n                    are important for shaping the avidity of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell responses. In the absence of T\n                    <jats:sub>regs<\/jats:sub>\n                    , CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell responses were of lower avidity, and the CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells were more responsive to lower-affinity antigens. When T\n                    <jats:sub>regs<\/jats:sub>\n                    were absent, stable interactions between T cell and antigen-presenting cells were increased as a result of higher amounts of chemokine expression in the lymph nodes. T\n                    <jats:sub>reg<\/jats:sub>\n                    depletion also resulted in a lower-avidity CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell response to infection with the bacterial pathogen\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1126\/science.1227049","type":"journal-article","created":{"date-parts":[[2012,10,25]],"date-time":"2012-10-25T15:31:32Z","timestamp":1351179092000},"page":"532-536","source":"Crossref","is-referenced-by-count":156,"title":["Regulatory T Cells Increase the Avidity of Primary CD8\n                    <sup>+<\/sup>\n                    T Cell Responses and Promote Memory"],"prefix":"10.1126","volume":"338","author":[{"given":"Luigia","family":"Pace","sequence":"first","affiliation":[{"name":"INSERM U932, Immunity and Cancer, Institut Curie, F-75248 Paris Cedex 05, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andy","family":"Tempez","sequence":"additional","affiliation":[{"name":"INSERM U932, Immunity and Cancer, Institut Curie, F-75248 Paris Cedex 05, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catharina","family":"Arnold-Schrauf","sequence":"additional","affiliation":[{"name":"Institute of Infection Immunology, Centre for Experimental and Clinical Infection Research, TWINCORE, D-30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabrice","family":"Lemaitre","sequence":"additional","affiliation":[{"name":"INSERM U668, Department of Immunology, Institut Pasteur, F-75015 Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe","family":"Bousso","sequence":"additional","affiliation":[{"name":"INSERM U668, Department of Immunology, Institut Pasteur, F-75015 Paris, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luc","family":"Fetler","sequence":"additional","affiliation":[{"name":"CNRS UMR 168, Laboratoire de Physico-Chimie Curie, Institut Curie, F-75248 Paris Cedex 05, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim","family":"Sparwasser","sequence":"additional","affiliation":[{"name":"Institute of Infection Immunology, Centre for Experimental and Clinical Infection Research, TWINCORE, D-30625 Hannover, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Amigorena","sequence":"additional","affiliation":[{"name":"INSERM U932, Immunity and Cancer, Institut Curie, F-75248 Paris Cedex 05, 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