Figure 2
Figure 2. Ruxolitinib inhibits IL-10–dependent macrophage polarization. (A) MDMs were generated and polarized with IL-10 as before. Cultures were supplemented with vehicle control (dimethylsulfoxide) or ruxolitinib (1 μM), and CD163, CD16, and HLA-DR expression was determined. (B-C) Polarized macrophages generated in the presence or absence of ruxolitinib (Rux) were washed with fresh media. (B) Media supplemented with lipopolysaccharide (100 ng/mL) were added, and cell-free supernatants were collected 24 hours later for determination of IL-10 production by cytometric bead array assay. The mean (±standard error) from 6 individual normal donors is shown. (C) In parallel, CFSE-labeled T cells were added in triplicate, and T-cell proliferation was determined by CFSE dilution. *P < .05 and **P < .01 in unpaired 2-sided Student t test.

Ruxolitinib inhibits IL-10–dependent macrophage polarization. (A) MDMs were generated and polarized with IL-10 as before. Cultures were supplemented with vehicle control (dimethylsulfoxide) or ruxolitinib (1 μM), and CD163, CD16, and HLA-DR expression was determined. (B-C) Polarized macrophages generated in the presence or absence of ruxolitinib (Rux) were washed with fresh media. (B) Media supplemented with lipopolysaccharide (100 ng/mL) were added, and cell-free supernatants were collected 24 hours later for determination of IL-10 production by cytometric bead array assay. The mean (±standard error) from 6 individual normal donors is shown. (C) In parallel, CFSE-labeled T cells were added in triplicate, and T-cell proliferation was determined by CFSE dilution. *P < .05 and **P < .01 in unpaired 2-sided Student t test.

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