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. 2024 Feb 6;15:899. doi: 10.1038/s41467-024-45056-x

Fig. 10. Sm-TCR Treg-dependent in vivo suppression of Sm+ lupus donor PBMC.

Fig. 10

a Experimental timeline for in vivo NSG-MHCnull mouse model of disease. Patient PBMCs, mature DCs pulsed with SmB/B’58-72 peptide and Tregs (mock polyclonal or Sm-specific) were administered on day 0, day 7, and day 21, respectively. b Proteinuria scores measured by urine test strips from mice administered no Tregs (brown), polyclonal Tregs (pTregs, blue), Sm-Tregs (green) or healthy control cells (purple) at week 3 and week 8. c Assessments of histological renal injury show the percentage of glomeruli affected by necrosis, d glomerular hypercellularity, e mesangial cell proliferation, and f tubulointerstitial injury from mice administered no Tregs (brown), polyclonal Tregs (pTregs, blue), Sm-Tregs (green), or healthy control cells (purple) at week 8. bf Data are presented as mean with SD. n = 5 independent experiments for mice receiving SLE patient cells and n = 4 for mice receiving healthy donor cells. *P < 0.0332, **P < 0.0021, ***P < 0.0002, ****P < 0.0001 by ordinary one-way ANOVA and Tukey’s multiple comparisons test. g Representative glomeruli from periodic acid Schiff (PAS)-stained kidney sections from mice administered no Tregs, polyclonal Tregs, Sm-Tregs or healthy control cells at week 8. Black arrows indicate areas of glomerular segmental necrosis. Source data are provided as a Source Data file. Created with Biorender.com.