Journal: bioRxiv

Article Title: IL-17A-driven Macrophage Disorder Promotes Plaque Instability in Psoriatic Atherosclerosis

doi: 10.1101/2025.05.21.654491

Figure Lengend Snippet: a, Changes in various lipid components in macrophages after IL-17A intervention. b-c, Enrichment analysis showing the main downregulated lipid types. d, Gene interaction network showing that PPARG is involved in three enrichment pathways: lipid homeostasis□cytokine-mediated signaling pathway□myeloid leukocyte differentiation. e, mRNA expression levels of PPARG, TREM2 in macrophages after IL-17A intervention. f, Immunofluorescence showing the spatial relationship between IL-17RA and PPARγ. g, mRNA expression levels of CXCL2, CXCL8, and TREM2 in macrophages after PPARγ agonist intervention. Significance indicated as *P < 0.05, **P < 0.01, ***P < 0.001, with ns denoting not significant. Statistical analysis was performed using the One-way ANOVA.

Article Snippet: Primary antibodies included mouse anti-CD68 (GB12192, Servicebio), mouse anti-PPARγ (sc-136250, Santa Cruz Biotechnology), and rabbit anti-MIP2 (GB11130, Servicebio).

Techniques: Expressing, Immunofluorescence

Journal: bioRxiv

Article Title: IL-17A-driven Macrophage Disorder Promotes Plaque Instability in Psoriatic Atherosclerosis

doi: 10.1101/2025.05.21.654491

Figure Lengend Snippet: a, mRNA expression levels of CD80, CD86 in macrophages after PPARγ agonist and IL-17A intervention. b, CD86 protein expression levels in macrophages after PPARγ agonist and IL-17A intervention. c, mRNA expression levels of CXCL2, CXCL3, CXCL8, CCL2, and CCL3 in macrophages after PPARγ agonist and IL-17A intervention. d, mRNA expression levels of TREM2,PLTP,APOE,FABP3 and FABP5 in macrophages after PPARγ agonist and IL-17A intervention. Significance indicated as *P < 0.05, **P < 0.01, ***P < 0.001, with ns denoting not significant. Statistical analysis was performed using the One-way ANOVA.

Article Snippet: Primary antibodies included mouse anti-CD68 (GB12192, Servicebio), mouse anti-PPARγ (sc-136250, Santa Cruz Biotechnology), and rabbit anti-MIP2 (GB11130, Servicebio).

Techniques: Expressing

Journal: bioRxiv

Article Title: IL-17A-driven Macrophage Disorder Promotes Plaque Instability in Psoriatic Atherosclerosis

doi: 10.1101/2025.05.21.654491

Figure Lengend Snippet: a, RNA sequencing data showing mRNA changes in mouse bone marrow primary macrophages after IL-17A inhibition. b, GO enrichment analysis of differential genes in bone marrow primary macrophages between IL-17A inhibitor-treated and control groups. c, KEGG enrichment analysis of differential genes in bone marrow primary macrophages between IL-17A inhibitor-treated and control groups. d, Immunofluorescence showing changes in MIP2 and PPARγ in the abdominal aorta between IL-17A inhibitor-treated and control groups. Significance indicated as *P < 0.05, **P < 0.01, ***P < 0.001, with ns denoting not significant. Statistical analysis was performed using the t-test.

Article Snippet: Primary antibodies included mouse anti-CD68 (GB12192, Servicebio), mouse anti-PPARγ (sc-136250, Santa Cruz Biotechnology), and rabbit anti-MIP2 (GB11130, Servicebio).

Techniques: RNA Sequencing, Inhibition, Control, Immunofluorescence

Journal: bioRxiv

Article Title: IL-17A-driven Macrophage Disorder Promotes Plaque Instability in Psoriatic Atherosclerosis

doi: 10.1101/2025.05.21.654491

Figure Lengend Snippet: Psoriasis mediates atherosclerotic plaque destabilization through IL-17A–IL-17RA–mediated downregulation of PPARγ in macrophages, leading to macrophage disorganization characterized by increased inflammation, production of inflammatory factors, and downregulation of sphingomyelin components.

Article Snippet: Primary antibodies included mouse anti-CD68 (GB12192, Servicebio), mouse anti-PPARγ (sc-136250, Santa Cruz Biotechnology), and rabbit anti-MIP2 (GB11130, Servicebio).

Techniques: