Fig. 3

Tertiary lymphoid organs in the mouse kidney after ischemia/reperfusion injury. a–d Periodic acid-Schiff (PAS) staining of representative mouse kidney sections 16 months after IRI (b–d) or age-matched controls (a); n = 3/group; scale bar = 500 μm in (a, b), 100 μm in (c), and 50 μm in (d). e Glomerular filtration rate (GFR), as measured by sinistrin clearance, in 7 mice 16–18 months after IRI and in 5 age-matched controls. Mann–Whitney test, **P < 0.01. f Semi-quantitative evaluation of immune cell infiltrates in the kidney at different time points after IRI or sham surgery as determined by CIBERSORT analysis on whole kidney RNAseq data. Mean values and SE are shown, n = 3/group. g, h Immunostaining of consecutive sections obtained from a representative mouse kidney 6 months after IRI (n = 3–4/group). CD31: endothelial cells; Havcr1 (Kim1): marker of tubular injury; Ltl: proximal tubule. CD45R: B cells (and a subset of T cells, s. Supplementary Fig. 2); CD21 and Cxcl13: follicular dendritic cells. i Higher magnification of the B cell zone highlighting the partial separation of germinal centers in two areas: upper part with Ki67⁺ proliferating cells, lower part with CD21⁺ follicular dendritic cells. j Cluster analysis of cytokine transcripts obtained from RNAseq data from renal tissue at different time points after IRI (n = 3 for each time point). k Cell specific expression analysis of cytokine transcripts from RNAseq data obtained after TRAP from Foxd1-derived renal stroma cells and Lyz2-derived myeloid cells at 28 days after IRI. The ratio of the mean RPKM values (Foxd1/Lyz2) obtained from 3 independent mice, including cytokine genes involved in the late immune response according to panel (j) are shown. Genes specifically expressed in myeloid cells are shown in blue and in stroma cells in red