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. Author manuscript; available in PMC: 2019 May 20.
Published in final edited form as: Clin Immunol. 2015 Nov 26;162:100–106. doi: 10.1016/j.clim.2015.11.010

Figure 1.

Figure 1

MiR-21 deficiency alleviates cGVHD-induced autoimmunity. cGVH reactions were induced in age- and sex matched wild-type (WT) and miR-21-deficient (miR-21−/−) hosts by in vivo transfer of 100 x 106 purified bm12 splenocytes. (A) MiR-21 deficiency ameliorates cGVH-induced splenomegaly. Mean WT and miR-21−/− spleen masses 6-weeks post-induction. n = nine independent experiments (B) representative spleen images demonstrating ameliorated splenomegaly in miR-21−/− host mice. (C) MiR-21 regulates autoantibody production. Blood samples were collected pre-induction (I) and at 6-weeks post-cGVH induction (F) and the sera assayed by ELISA for anti-double-stranded DNA antibodies as described in Materials and Methods. n = 6 independent experiments and (D) MiR-21 deficiency reduces immune complex-mediated nephrotic proteinuria. Urine samples were collected pre-induction (I) and at 6-weeks post-cGVH induction (F) and assayed for total urine protein as described in Materials and Methods. n = nine independent experiments. *p < 0.05 and **p < 0.01 by Mann–Whitney unpaired t test.