Fig. 5: Treatment of SAR131675 decreases tertiary lymphoid organ formation and inflammatory cytokine expression in resiquimod-induced lupus nephritis. | Cell Death Discovery

Fig. 5: Treatment of SAR131675 decreases tertiary lymphoid organ formation and inflammatory cytokine expression in resiquimod-induced lupus nephritis.

From: Inhibition of VEGFR-3 by SAR131675 decreases renal inflammation and lymphangiogenesis in the murine lupus nephritis model

Fig. 5

A Representative sections of kidneys from each experimental group of SAR131675 treatment in the resiquimod-induced LN were co-stained with B220/CD3, B220/CD21, LYVE-1/B220, LYVE-1/PNAd. TLOs formation is reduced, and renal function is improved after treatment with SAR131675. Scale bar = 50 μm. B Representative mRNA analysis of proinflammatory cytokines and chemokine expression. Expression levels are normalized to Gapdh. Statistical significance was determined using one-way ANOVA followed by Tukey’s post-hoc test. Data are expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 versus each group. Control, vehicle-treated group; SAR, SAR131675-treated group; Lupus, resiquimod-treated group; Lupus+SAR, resiquimod and concomitantly SAR131675-treated group. DAPI 4’,6-diamidino-2-phenylindole, LN lupus nephritis, LYVE-1 lymphatic vessel endothelial hyaluronan receptor-1, PNAd peripheral node addressin, Ccl19 C-C motif chemokine ligand 19, Ccl21 C-C motif chemokine ligand 21, Cxcl13 C-X-C motif chemokine ligand 13, Mcp-1 monocyte chemoattractant protein-1, Ccr7 C-C chemokine receptor type 7, Icam-1 intercellular adhesion molecule-1, Vcam-1 vascular cell adhesion molecule 1, Ltβ lymphotoxin beta, Baff B-cell activating factor, GAPDH glyceraldehyde 3-phosphate dehydrogenase.

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