{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martelossi Cebinelli GC"],"funding":["State of Sao Paulo Research Foundation"],"pagination":["112083"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12003019"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(4)"],"pubmed_abstract":["The dysregulated host response to infections can lead to sepsis, a complex disease characterized by a spectrum of clinical phenotypes. Using scRNA-seq, we analyzed the immune cell of survived and non-survived CLP-septic mice to gain insights into the immunological mechanisms by which neutrophils contribute to the hyperinflammatory phenotype. Our findings reveal that non-survived mice exhibit increased frequencies of immature CXCR4<sup>+</sup> PD-L1<sup>+</sup> neutrophils in the bloodstream, accompanied by an accumulation of trafficking-specific CXCR4<sup>+</sup> PD-L1<sup>+</sup> neutrophils into the lungs. The IFN-gamma and LPS promote the PD-L1 expression on neutrophils and an activation profile associated with inflammation and organ damage. Notably, abrogating the IFN-gamma reduced sus"],"journal":["iScience"],"pubmed_title":["CXCR4&lt;sup&gt;+&lt;/sup&gt; PD-L1&lt;sup&gt;+&lt;/sup&gt; neutrophils are increased in non-survived septic mice."],"pmcid":["PMC12003019"],"funding_grant_id":["2013/08216-2","2019/15070-0"],"pubmed_authors":["Ramos ADS","Tavares AC","Bernardo Nascimento DC","Alves Damasceno LE","Alves de Lima K","Aquime Goncalves AN","Cunha TM","Imoto Nakaya HT","Martelossi Cebinelli GC","Alves-Filho JC","de Oliveira Leandro M","da Cruz Oliveira Barros C","Rocha Oliveira AE","Cunha FQ","Donate PB","Costa V"],"additional_accession":[]},"is_claimable":false,"name":"CXCR4&lt;sup&gt;+&lt;/sup&gt; PD-L1&lt;sup&gt;+&lt;/sup&gt; neutrophils are increased in non-survived septic mice.","description":"The dysregulated host response to infections can lead to sepsis, a complex disease characterized by a spectrum of clinical phenotypes. Using scRNA-seq, we analyzed the immune cell of survived and non-survived CLP-septic mice to gain insights into the immunological mechanisms by which neutrophils contribute to the hyperinflammatory phenotype. Our findings reveal that non-survived mice exhibit increased frequencies of immature CXCR4<sup>+</sup> PD-L1<sup>+</sup> neutrophils in the bloodstream, accompanied by an accumulation of trafficking-specific CXCR4<sup>+</sup> PD-L1<sup>+</sup> neutrophils into the lungs. The IFN-gamma and LPS promote the PD-L1 expression on neutrophils and an activation profile associated with inflammation and organ damage. Notably, abrogating the IFN-gamma reduced sus","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-01T07:52:06.8Z","creation":"2026-04-08T10:40:26.159Z"},"accession":"S-EPMC12003019","cross_references":{"pubmed":["40241761"],"doi":["10.1016/j.isci.2025.112083"]}}