Skip to main content
. Author manuscript; available in PMC: 2018 Nov 15.
Published in final edited form as: J Immunol. 2017 Oct 6;199(10):3525–3534. doi: 10.4049/jimmunol.1701011

FIGURE 7.

FIGURE 7

IFN-β and B. burgdorferi are both required for the enhanced expression of myostatin by CD45− joint cells during infection and ex vivo. (A) In vivo mAb blocking of IFN-β (600 μg total) prevents transcriptional upregulation of Mstn in CD45− joint cells from ISRCL4 and ISRCL3 mice 22 days post infection with B. burgdorferi (n = 3 to 4 samples per group, each sample was comprised of cells from both rear ankle joints pooled from two mice). Mstn transcripts were normalized to β-actin and fold change relative to isotype control was calculated for each strain. Significance determined by unpaired Student’s t test. *p < 0.05, **p < 0.01. (B) Ex vivo administration of exogenous IFN-β (100 U/ml) in combination with B. burgdorferi (10:1 MOI) for 3 h caused transcriptional upregulation of Mstn in CD45− cells isolated from a naïve B6 mouse joint. Transcripts were normalized to β-actin and fold change was calculated relative to media control. Results are pooled data from two experiments using CD45− cells from 8 or more mice done on separate days (n = 5 wells per group). Significance determined by 1-way ANOVA followed by Dunnett’s multiple comparison test versus media. *p < 0.05.