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. Author manuscript; available in PMC: 2011 Jun 17.
Published in final edited form as: Nature. 2010 Jun 17;465(7300):937–941. doi: 10.1038/nature09102

Figure 4. PDCs from lupus-prone mice have intrinsic resistance to glucocorticoid-induced cell death compared to normal mice because of TLR7 and 9 activation by self-nucleic acid.

Figure 4

a, b, Normal (closed symbols) and lupus-prone (open symbols) animals were either left untreated or treated with dexamethasone (GC). Cell numbers in blood (a, fold change to pre-bleed) and spleens (b, fold change to untreated) was assessed 18 h later. Cumulative data of at least three independent experiments is shown. *** P ≤ 0.001 indicate differences between both lupus strains from either normal strains. 129 and B6, normal mice; TLR7 and NZB, lupus-prone mice. c, d, (NZB×NZW)F1 and TLR7.Tg.6 mice (c and d, respectively) were left untreated or treated with glucocorticoids alone or in the presence of IRS or control (CTRL) ODN (100 μg per mouse sub-cutaneously) given every 3 days for 10 days before the glucocorticoid treatment. Viability was assessed in the spleen 18 h after DEX. Cumulative data of two independent experiments is shown.