Fig. 1: Common signatures of neutrophils in different disease conditions.

a UMAP plot of neutrophil transcriptional states in the pooled scRNA-seq dataset of the bone marrow, peripheral blood, spleen, and disease-inflicted tissues of different mouse models. GMP, granulocyte-monocyte progenitor. b Violin plots of the signature genes for neutrophil transcriptional states. c RNA velocity plot of neutrophil transcriptional states. d Pseudotime trajectory analysis of neutrophil transcriptional states. e, f UMAP plots of neutrophils in the diseased tissues (e) or the peripheral blood (f) of different mouse models. g Proportions of neutrophil transcriptional states in the bone marrow, peripheral blood, spleen, and diseased tissues of different mouse models. h Enrichment score heatmap of the gene sets of cytokine-related pathways in neutrophil transcriptional states. i, j C57BL/6 wild-type or Ifngr1^–/– mice (i) or Rag2^–/– and Rag2 ^–/– Il2rg^–/– mice (j) were subjected to ALI. Total neutrophils in the peripheral blood, spleen, and lung tissues and their mean fluorescence intensity (MFI) of Cd274 expression were assessed by FACS. Data are shown as mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001 (ANOVA test). k BALB/c wild-type or nude mice were utilized in the LCPNS-SIIN glioma model. Total neutrophils and Cd274⁺ neutrophils in the bone marrow, peripheral blood, spleen, and tumors were examined by FACS. Data are shown as mean ± SD; *P < 0.05, **P < 0.01 (ANOVA test). l, m C57BL/6 wild-type mice were subjected to ALI (l) or LCPNS-SIIN gliomas (m). MFI of Cd244, Il4ra, or Cd101 expressed by neutrophils in the peripheral blood was quantified by FACS. Data are shown as mean ± SD; ns not significant, **P < 0.01 (Student’s t-test).