Fig 2: PD1 blockade does not reverse ATT impairment.(A) Schematic of in vivo PD1 blockade timeline and interventions. (B) Glucose tolerance test of ND- and HFD-fed mice after administration of aPD1 or IgG2a isotype injections (left) and glucose levels after fasting for 6 hours (right). n = 4 biological replicates/group, analyzed by 2-way ANOVA where *P < 0.05, **P < 0.01. (C and D) ATT activation assays were performed on eWAT SVF and splenocytes after PD1 blockade regimen. Frequency of CD25 expression on CD8+ T cells and Tconv measured 3 days after Dynabead stimulation. n = 4 biological replicates/group, analyzed by 2-way ANOVA where *P < 0.05, **P < 0.01, ****P < 0.0001. (E and F) IL-2 and IFN-? concentration in culture supernatants from PD1 blockade ATT activation assays of eWAT SVF and splenocytes. n = 4 biological replicates/group, analyzed by 2-way ANOVA.

Fig 3: Representative images for H&E of lungs are shown for control, granuloma, granuloma treated with MIA602 and granuloma treated with methylprednisolone (a). Percentage differences of lung-stained cells for different markers (CD30, CD68, PD-1 and PD-L1) between challenged mice and controls (b). Control mice (three mice) were not challenged, while granuloma (four mice) and MIA602 (three mice) groups were challenged with MAB microparticles. Mice in the MIA602 group received 5 µg MIA602 daily subcutaneous injection, while granuloma and control groups only received saline. The percentage of the involved area of the immunohistochemistry was evaluated by two lung pathologists separately. Data are from one experiment that is representative of three separate experiments.