Fig. 4: Myeloid Tshr deficiency suppresses M1 polarization of macrophages and the secretion of IL-1α, IL-1β and IL-6.

Tshr^f/f- or Tshr^MKO-derived BMDMs were stimulated by 1 ng/mL TSH for 24 h, and flow cytometry was then performed to analyze the effects of myeloid Tshr deficiency on M1 polarization of macrophages and intracellular ROS levels. a CD80⁺ M1 macrophages from the CD11b⁺ F4/80⁺ cell gate (n = 3). b Intracellular ROS levels (left) and mean fluorescence intensity (MFI) of ROS (right) (n = 3). c A heatmap of the proinflammatory cytokines in Tshr^f/f- or Tshr^MKO-derived BMDMs determined by mRNA sequencing. d The mRNA levels of the proinflammatory cytokines in the above BMDMs were measured by qRT-PCR. β-Actin was used as an internal control (n = 9). Tshr^MKO mice and age-matched Tshr^f/f littermates (male, 6 weeks old) were fed with HFD for 9 weeks. Serum concentrations of IL-1α (e), IL-1β (f) and IL-6 (g) in these mice were then measured by ELISA (n = 6). h qRT-PCR assays were performed to determine mRNA levels of Il-1a, Il-1b and Il-6 in Tshr^f/f- or Tshr^MKO-derived BMDMs stimulated by 1 ng/mL TSH for 24 h. β-Actin was used as an internal control (n = 3). Data are presented as mean ± s.d. **P < 0.01, ***P < 0.001 (unpaired two-tailed Student’s t-test for a, b and e–g; one-way ANOVA for d and h).