Figure 3.

MIF inhibition induces a DC phenotype in MDSCs derived from a patient with melanoma.

(A) Aberrant accumulation of MDSCs in patients with late‐stage melanoma (stage III/IV) may represent an essential mechanism of immediate and/or acquired resistance to IPI and/or nivolumab (NIVO) immune checkpoint inhibitors. (B) Therapeutic targeting of MIF with 4‐IPP, a highly efficacious and orally bioavailable, small‐molecule MIF antagonist, attenuates MDSC immune suppression derived from patients with melanoma. Importantly, 4‐IPP induces a functional MDSC → DC‐like differentiation and thus, can attenuate the MDSC‐mediated resistance to immunotherapies.