Fig 2: Impact of CAR T cells and FA-TLR7-1A on the properties of tumor infiltrating TAMs and MDSCs. (A) Estimation of the M1:M2 ratios of F4/80 positive macrophages within the solid 4T1-mCD19 tumors following treatment with the indicated therapies. The ratio of inducible nitric oxide synthase (iNOS) to arginase 1 (Arg 1) was used as an estimate of M1-like to M2-like macrophages. (B) Percentage of live CD45+ cells in the solid tumors that were F4/80 positive macrophages. (C) Percentage of MDSCs in live CD45+ cells in the solid tumors. (D) Ratio of the iNOS+ to Arg 1+ population among live MDSCs. (E) Percentage of the iNOS+ population in live MDSCs. (F) Percentage of Arg 1+ population in live MDSCs. This study was performed three times with similar results each time. The number of mice/group is the same as reported in the legend to Figure 3 , except in the CAR-T + 3 nmol FA-TLR7-1A, 5/W group only 5 of 9 tumors could be analyzed because 4 of 9 mice experienced complete cures. Mean ± SEM. Statistical significance was determined using an unpaired two-tailed t-test (*P < 0.05, ***P < 0.001, ns, not significant P = 0.05).

Fig 3: ADNP-deficient mice have reduced antigen-specific Th2 cell responses(A) Schematic of the experimental induction of type 2 inflammation in the mouse lung with papain and 2W1S peptide.(B–H) Flow cytometric analysis of lung (B) total Th effector cells, (C) total and 2W1S-tetramer-specific IL-13-producing Th effector cells, (D) total and 2W1S-tetramer-specific IL-5-producing Th effector cells, (E) total IFN-? and IL-17A-producing Th effector cells, (F) GATA3 expression in Th2 cells, (G) Arg1 expression in Arg1+CD11b+ dendritic cells (DCs), and (H) serum IgE quantified by ELISA. Data are representative of 2 independent experiments; mean ± SD; one-way ANOVA with Tukey’s post-hoc test. ***p < 0.001, **p < 0.01, *p < 0.05, not significant (ns).(I–L) Flow cytometric analysis of lung (I) total and 2W1S-tetramer-specific IL-13-producing Th effector cells and total IL-5-producing Th effector cells, (J) total M2 macrophage and Arg1 expression in M2 macrophage, (K) total bronchoalveolar eosinophils, (L) total CD11b+ and Arg1+CD11b+ DCs and Arg1 expression in Arg1+CD11b+ DCs. Data are representative of 2 independent experiments; mean ± SD; one-way ANOVA with Tukey’s post-hoc test. ****p < 0.0001, **p < 0.01, *p < 0.05.See also Figures S1 and S2.

Fig 4: CUR promotes polarization and reverses PRV-induced mitochondrial dysfunction in PRV-infected BV2 cells. BV2 cells were infected with/without PRV for 24 h and then treated with/without 20 µM CUR for 24 h. A The expression of the M1 phenotype surface markers CD40 and CD16/32 and B the M2 phenotype surface markers CD206 and ARG-1 in BV2 cells was determined using flow cytometry (n = 3). C Mitochondrial structures in BV2 cells were observed using transmission electron microscopy (n = 3); scale bar = 500 nm. D Mitochondrial membrane potential (MMP) in BV2 cells. E MMP in BV2 cells was observed using fluorescence microscopy (n = 4); scale bar = 200 µm. All experiments were performed in parallel. The results are presented as the mean ± SD. Statistical significance was determined using one-way ANOVA followed by an LSD post hoc test for multiple comparisons among the groups. *P < 0.05, **P < 0.01, ***P < 0.001, and NS, not significant.