Fig. 7
IL-33 enhances kidney ILC2s and renal function in lupus nephritis. A Experimental design of in vivo ILC2 expansion in the IMQ model. B Survival kinetics of the IL-33-treated IMQ model mice (n = 14). C Glomerular size in the IL-33-treated IMQ model mice was assessed using H&E staining (n = 7–10). D Gene expression levels of Ifng, Il17a, Il1b, Il6, and Ccl2 in renal tissue were quantified using RT‒qPCR (n = 7‒9). E Frequencies of ILCs in the IMQ model mice after IL-33 treatment (n = 10–13). F, G Flow cytometry analysis of the expression of integrin α4 (F) and β7 (G) in kidney ILC2s (n = 3–5). H Glomerular size in the ILC2 adoptive transfer (ivILC2) or rAREG treated IMQ model mice was assessed using H&E staining (n = 6–11). I Experimental design of the in vitro assay in which splenic CD4+ T cells from old MRL-lpr mice and IL-33-treated kidney ILC2s from young MRL-lpr mice were cocultured. J Frequencies of IFN-γ and IL-17A in splenic CD4+ T cells from old MRL-lpr mice cocultured with IL-33-treated kidney ILC2s from young MRL-lpr mice. K Comparison of Areg expression between ILC2s and CD4+ T cells from cocultures (n = 5). All results are shown as the means ± SEMs, and the statistical analysis was performed using the Mann‒Whitney U test or Kruskal‒Wallis test. ns not significant; *P < 0.05; **P < 0.01; and ****P < 0.0001
