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. Author manuscript; available in PMC: 2018 Nov 16.
Published in final edited form as: Nature. 2018 May 16;557(7706):580–584. doi: 10.1038/s41586-018-0125-z

Fig. 1 |. Tet2 deficiency leads to systemic bacterial dissemination.

Fig. 1 |

a, In vitro HSC self-renewal colony-forming assay of haematopoietic progenitors (n = 3 mice). Mean ± s.e.m. b, Bacterial 16S gene copies in peripheral blood (left; n = 4, 10 and 37 for germ-free wild-type (WT), Tet2+/+ and Tet2−/− mice, respectively), MLN (middle; n = 4, 11 and 15 for germ-free wild-type, Tet2+/+ and Tet2−/− mice, respectively) and spleen (right; n = 4, 11 and 19 for germ-free wild-type, Tet2+/+ and Tet2−/− mice, respectively). Germ-free wild-type mice served as negative control. Centre at median, two-tailed Mann–Whitney U-test. Bacterial 16S rRNA gene qPCRs from about 30 mg MLN and about 30 mg spleen were normalized to the host murine Ifnbl gene. c, Correlation between 16S gene copies in the peripheral blood and numbers (left) or frequency (right) of peripheral-blood CD11b+Gr1+myeloid cells (n = 40 mice). Pearson correlation test. d, Representative image of aerobic and anaerobic cultures. e, f, Quantification of bacteria colony-forming units (CFUs) of MLN and spleen suspensions grown under anaerobic (e) or aerobic (f) conditions. In b, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Data are representative of at least three independent experiments.