Fig. 4: Maintenance of remission by the Irf5 cKO in the Lyn-deficient mouse model of SLE.
From: Genetic and chemical inhibition of IRF5 suppresses pre-existing mouse lupus-like disease

a The LLPC number in bone marrow (BM; left) or in the spleen (right) from WT (n = 17), Lyn−/−Irf5fl/fl (n = 10), and Lyn−/−Irf5fl/flCreER (n = 12) mice at 24–28 weeks after TAM treatment as in Fig. 3a (40–46 weeks of age) was analyzed by flow cytometry. b The scheme of the Irf5 cKO combined with BZ-induced LLPC depletion; s.c. subcutaneously. c, d Irf5 and ISG expression. Irf5 (c) and Oasl2 (d) mRNA levels in peripheral blood from Lyn−/−Irf5fl/fl (n = 11) and Lyn−/−Irf5fl/flCreER (n = 7) female and male mice (29–32 weeks of age at week 0) treated as in b were analyzed by RT-qPCR. e The LLPC number in BM (left) and spleen (right) from WT (n = 8), Lyn−/−Irf5fl/fl (n = 10), and Lyn−/−Irf5fl/flCreER (n = 6) mice at 12 weeks after the first injection (41–44 weeks of age) as in b was analyzed by flow cytometry. f Spleen weight of mice in e. The circles and diamonds denote the female and male mice, respectively. g Autoantibody production. Serum anti-dsDNA IgG from mice in c was quantified by ELISA. Data were pooled from two independent experiments. Horizontal bars (a, c–g) indicate mean ± SEM. Dashed lines (c, d, g) denote mean data from WT mice (n = 5). *P < 0.05, **P < 0.01, ***P < 0.001 (two-sided Student’s t test in a, e, f; two-sided paired t test in c, d, g).