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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Arthritis Rheumatol. 2018 Apr 18;70(6):855–867. doi: 10.1002/art.40447

Figure 5. IL-22 deficiency and αIL-17 treatment partially ameliorated the bone defects in R26STAT3Cstopfl/fl CD4Cre mice.

Figure 5

(A) MicroCT analysis on the femur of R26STAT3Cstopfl/fl CD4Cre mice and their littermate controls that were crossed onto IL-22−/− background or treated with αIL-17. The 3D images showing femur bones of these mice (left) with trabecular and cortical thickness of these animals quantified (right). (B) Percentage of CD3+ CD4+ cells that produce IL-17 in the bone marrow of R26STAT3Cstopfl/fl CD4Cre mice and their littermate controls that were crossed onto IL-22−/− background or treated with αIL-17. (C–D) Percentage of osteoclast progenitor cells and RANKL producers in the bone marrow of IL-22−/− and αIL-17 treated mice. Analysis was performed on mice aged between 6 to 10 weeks old. Number of independent experiments ≥ 3 for all assays. Statistical significance was assessed using the nonparametric two-tailed Mann-Whitney U test. Significance values are as follows: ns p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p ≤ 0.0001.