CXCR4⁺ PD-L1⁺ neutrophils are increased in non-survived septic mice.

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⁺ PD-L1⁺ neutrophils in the bloodstream, accompanied by an accumulation of trafficking-specific CXCR4⁺ PD-L1⁺ 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

SUBMITTER: Martelossi Cebinelli GC 

PROVIDER: S-EPMC12003019 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature