Fig. 1
From: Context-specific regulation of surface and soluble IL7R expression by an autoimmune risk allele

LPS induces profound monocyte IL7R cell surface expression. a Representative flow cytometry plots from live gated positively selected CD14 monocytes from one individual where cells were incubated for 24 h alone (top panel) or in presence of LPS (bottom panels). b Violin plot demonstrating significant induction of IL7R+ monocytes in paired cultures of positively selected monocytes (Monocyte IL7R+ post LPS- median: 23.8, min: 6.5, max: 55.8, IQR: 15.6–34.9%; n = 84, paired t-test). c Comparative effects of LPS on IL7R+ counts across CD14+ monocytes, CD4+ and CD8+ T cells, and CD56+ NK cells from the same PBMC cultures, untreated or with LPS for 24 h (PBMC IL7R+ post LPS-median: 29.9%, min: 5.9, max: 66.40, IQR: 22.3–40.0; n = 103, paired t-test). d Pearson correlation analyses were performed between indicated cells and treatments on number of IL7R+ cells. ***P < 0.001, **P < 0.01. e Comparative induction of IL7R+ monocytes from 6 individuals with monocytes treated for 24 h with either the TLR7 agonist Imiquimod, TLR1/2 agonist Pam3CysK4 or TLR4 agonist LPS (paired t-tests). Error bars show mean, IQR, min and max. f Array derived RNA expression of TNF at 2 h LPS assayed versus RNA expression of IL7R from monocytes from same individuals at 24 h LPS. g Comparative incubation of monocytes alone (n = 69), with LPS or with LPS + anti-TNF monoclonal antibody (Infliximab). Incubation with TNF antagonist significantly reduces LPS induced IL7R+ monocyte counts (paired t-test). h Violin plots of responses across cell types of PBMCs treated with TNF alone leads to significant induction of IL7R+ monocytes and significantly reduces CD4 and CD8 T cell IL7R+ positivity (n = 78, paired t-test). Source data are provided as a Source Data file