(A) Flow cytometric analysis shows a higher percentage of CD45^–PDPN⁺CD31^– FRCs and proliferating (Ki67⁺) FRCs in KLNs harvested 2 days following IRI from Rag1^–/– mice injected with WT T cells than KLNs from those injected with LTα^–/– T cells, along with representative flow cytometry plots (gated on CD45^– cells) (n = 3–4/group, mean ± SEM). (B) H&E staining (scale bar: 75 μm) of kidney tissue from Rag1^–/– mice following IRI demonstrates renal protection upon adoptive T cell transfer from LTα^–/– mice, along with (C) lower BUN, as compared with Rag1^–/– mice that received T cells from WT mice (n = 3/group, mean ± SEM). (D) Immunofluorescence of KLN shows marked decrease in PDPN⁺ FRCs in DT-treated CCL19^Cre × iDTR mice as compared with untreated WT mice. Paucity in HEV abundance and abrogation of architectural elongation is also shown. Scale bars: 200 μm for PDPN, 100 μm for MECA79. (E) Absolute cell counts of FRCs and HEVs are significantly lower in the KLNs of CCL19^Cre × iDTR mice, in comparison with the KLNs from WT mice, as determined by flow cytometric analysis (n = 3/group, mean ± SEM). (F) FRC depletion leads to amelioration in kidney damage after IRI. H&E staining shows less tubular injury in CCL19^Cre × iDTR mice, as compared with WT mice. F4/80 staining indicates tissue inflammation is markedly decreased in CCL19^Cre × iDTR mice after IRI. LTL identifies proximal tubules. Scale bars: 75 μm. (G) Left panel: Mean cortical thickness of kidneys in FRC-depleted mice was higher than in WT mice following IRI (n = 6/group, mean ± SEM). Right panel: CCL19^Cre × iDTR mice are protected from IRI, as indicated by lower BUN (mg/dl) (n = 6/group, mean ± SEM). (H) Left panel: Absolute count of CD4⁺IFN-γ⁺ T cells in KLN is significantly lower in CCL19^Cre × iDTR mice in comparison with WT mice following IRI. Right panel: Absolute count of CD4⁺CD44^hi T cells in KLN is significantly lower in CCL19^Cre × iDTR mice in comparison with WT mice (n = 3–4/group, mean ± SEM). *P < 0.05; **P < 0.01 by Student’s t test.