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. 2021 Jul 13;54(7):1494–1510.e7. doi: 10.1016/j.immuni.2021.04.025

Figure 3.

Figure 3

ACKR1 is elevated in aged tissues and retains mast cell-derived CXCL1 at EC junctions

(A–G) Young and aged WT mice were treated i.s. with PBS or IL-1β and cremaster muscles analyzed by confocal microscopy.

(A) Representative confocal images of post-capillary venules (PCVs) immunostained for CD31 and CXCL1 (scale bar: 4 μm; dashed boxes delineate magnified areas) and (B) quantification of CXCL1 expression (MFI) at EC junctional (junc.) and non-junctional (non-junc.) regions (n = 6-7 mice/group).

(C) EC CXCL1 expression (MFI) in control and mast cell-depleted aged cremaster tissues (n = 3-5 mice/group). (D) Representative confocal images illustrating ACKR1 expression in PCVs (CD31; scale bar: 10 μm) and ACKR1 quantification (MFI) within (E) whole ECs, and EC (F) non-junctional or (G) junctional regions (n = 3 mice/group).

(H) Generation of EC Ackr1+/+ and EC Ackr1−/− chimeras. (I-K) Young and aged chimeras as generated in (H) were treated i.s. with IL-1β.

(I) Representative confocal images of cremasteric PCVs immunostained for CD31 and CXCL1 (scale bar: 4 μm), (J) quantification of CXCL1 expression (MFI) within EC junctional and non-junctional regions (n = 3-8 mice/group) and (K) plasma CXCL1 as quantified by ELISA (n = 3-8 mice/group). Means ± SEM, #p < 0.05, ##p < 0.01, ###p < 0.001 relative to controls, ∗p < 0.05, ∗∗p < 0.01, n.s. not significant, as indicated.

See also Figure S3.