<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gossez M</submitter><funding>European Research Council</funding><funding>Agence Nationale de la Recherche (French National Research Agency)</funding><pagination>3030</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11953283</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>Sepsis, a leading cause of death in intensive care units, is associated with immune alterations that increase the patients' risk of secondary infections and mortality, so better understandings of the pathophysiology of sepsis-induced immunosuppression is essential for the development of therapeutic strategies. In a murine model of sepsis that recapitulates immune alterations observed in patients, here we demonstrate that PD-L1&lt;sup>+&lt;/sup>CD44&lt;sup>+&lt;/sup>B220&lt;sup>Low&lt;/sup>CD138&lt;sup>+&lt;/sup>IgM&lt;sup>+&lt;/sup> regulatory plasma cells are induced in spleen and regulate ex vivo proliferation and IFNɣ secretion induced by stimulation of T splenocytes. This effect is mediated both by cell-cell contact through increased PD-L1 expression on plasma cells and by production of a soluble factor. These obse</pubmed_abstract><journal>Nature communications</journal><pubmed_title>PD-L1&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; plasma cells suppress T lymphocyte responses in patients with sepsis and mouse sepsis models.</pubmed_title><pmcid>PMC11953283</pmcid><funding_grant_id>ANR-20-CE92-0024-01</funding_grant_id><funding_grant_id>616986</funding_grant_id><pubmed_authors>Malcus C</pubmed_authors><pubmed_authors>Gossez M</pubmed_authors><pubmed_authors>Py BF</pubmed_authors><pubmed_authors>Pescarmona R</pubmed_authors><pubmed_authors>Carre C</pubmed_authors><pubmed_authors>Bequet F</pubmed_authors><pubmed_authors>Richard JC</pubmed_authors><pubmed_authors>Boussaha I</pubmed_authors><pubmed_authors>Gardiner D</pubmed_authors><pubmed_authors>Caruso L</pubmed_authors><pubmed_authors>Raychaudhuri A</pubmed_authors><pubmed_authors>Martin O</pubmed_authors><pubmed_authors>Tissot S</pubmed_authors><pubmed_authors>Oriol G</pubmed_authors><pubmed_authors>Truc C</pubmed_authors><pubmed_authors>Koenig N</pubmed_authors><pubmed_authors>Crozon-Clauzel J</pubmed_authors><pubmed_authors>Textoris J</pubmed_authors><pubmed_authors>Bounab Y</pubmed_authors><pubmed_authors>Huriaux L</pubmed_authors><pubmed_authors>Dailler F</pubmed_authors><pubmed_authors>Jourdan C</pubmed_authors><pubmed_authors>Mallet F</pubmed_authors><pubmed_authors>RICO study group</pubmed_authors><pubmed_authors>Debord-Peguet S</pubmed_authors><pubmed_authors>Gregoire A</pubmed_authors><pubmed_authors>Kandara K</pubmed_authors><pubmed_authors>REALISM study group</pubmed_authors><pubmed_authors>Mommert M</pubmed_authors><pubmed_authors>Bitker L</pubmed_authors><pubmed_authors>Gatel J</pubmed_authors><pubmed_authors>Grosjean C</pubmed_authors><pubmed_authors>Uberti T</pubmed_authors><pubmed_authors>Buisson M</pubmed_authors><pubmed_authors>Riffaud C</pubmed_authors><pubmed_authors>Berger SB</pubmed_authors><pubmed_authors>Devigne B</pubmed_authors><pubmed_authors>De Monfort A</pubmed_authors><pubmed_authors>Thaunat O</pubmed_authors><pubmed_authors>Vallin H</pubmed_authors><pubmed_authors>Coudereau R</pubmed_authors><pubmed_authors>Maucort-Boulch D</pubmed_authors><pubmed_authors>Genin C</pubmed_authors><pubmed_authors>Florin K</pubmed_authors><pubmed_authors>Brengel-Pesce K</pubmed_authors><pubmed_authors>Delignette MC</pubmed_authors><pubmed_authors>Lopez J</pubmed_authors><pubmed_authors>Moriceau F</pubmed_authors><pubmed_authors>Conti F</pubmed_authors><pubmed_authors>Gallet-Gorius E</pubmed_authors><pubmed_authors>Meuret P</pubmed_authors><pubmed_authors>Macnamara A</pubmed_authors><pubmed_authors>Moriniere J</pubmed_authors><pubmed_authors>Peleraux A</pubmed_authors><pubmed_authors>Villard M</pubmed_authors><pubmed_authors>Hengy B</pubmed_authors><pubmed_authors>Gillespie I</pubmed_authors><pubmed_authors>Toetsch S</pubmed_authors><pubmed_authors>Augris-Mathieu C</pubmed_authors><pubmed_authors>Collus M</pubmed_authors><pubmed_authors>Arnal 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N</pubmed_authors><pubmed_authors>Cejka JC</pubmed_authors><pubmed_authors>Rahali N</pubmed_authors><pubmed_authors>Faure A</pubmed_authors><pubmed_authors>Cortez P</pubmed_authors><pubmed_authors>Cour M</pubmed_authors><pubmed_authors>Defrance T</pubmed_authors><pubmed_authors>Fraisse L</pubmed_authors><pubmed_authors>Marcotte G</pubmed_authors><pubmed_authors>Blein S</pubmed_authors><pubmed_authors>Bertin-Maghit A</pubmed_authors><pubmed_authors>Bouffard Y</pubmed_authors><pubmed_authors>Davidson J</pubmed_authors><pubmed_authors>Leray V</pubmed_authors><pubmed_authors>Vedrine C</pubmed_authors><pubmed_authors>Groussaud M</pubmed_authors><pubmed_authors>Becker J</pubmed_authors><pubmed_authors>Lukaszewicz AC</pubmed_authors><pubmed_authors>Matray M</pubmed_authors><pubmed_authors>Cheynet V</pubmed_authors><pubmed_authors>Girardot T</pubmed_authors><pubmed_authors>Fayolle-Pivot L</pubmed_authors><pubmed_authors>Ber CE</pubmed_authors><pubmed_authors>Wallet 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F</pubmed_authors><pubmed_authors>Guichard A</pubmed_authors><pubmed_authors>Venet F</pubmed_authors><pubmed_authors>Tipple C</pubmed_authors><pubmed_authors>Lombard C</pubmed_authors></additional><is_claimable>false</is_claimable><name>PD-L1&amp;lt;sup&amp;gt;+&amp;lt;/sup&amp;gt; plasma cells suppress T lymphocyte responses in patients with sepsis and mouse sepsis models.</name><description>Sepsis, a leading cause of death in intensive care units, is associated with immune alterations that increase the patients' risk of secondary infections and mortality, so better understandings of the pathophysiology of sepsis-induced immunosuppression is essential for the development of therapeutic strategies. In a murine model of sepsis that recapitulates immune alterations observed in patients, here we demonstrate that PD-L1&lt;sup>+&lt;/sup>CD44&lt;sup>+&lt;/sup>B220&lt;sup>Low&lt;/sup>CD138&lt;sup>+&lt;/sup>IgM&lt;sup>+&lt;/sup> regulatory plasma cells are induced in spleen and regulate ex vivo proliferation and IFNɣ secretion induced by stimulation of T splenocytes. This effect is mediated both by cell-cell contact through increased PD-L1 expression on plasma cells and by production of a soluble factor. These obse</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2026-06-02T12:00:18.167Z</modification><creation>2026-04-18T03:10:52.128Z</creation></dates><accession>S-EPMC11953283</accession><cross_references><pubmed>40155394</pubmed><doi>10.1038/s41467-025-57706-9</doi></cross_references></HashMap>