Inhibition of the interaction between MIF and CD74 via ibudilast treatment results in reduced downstream signaling of MCP-1, which has been shown to be MIF-dependent in studies of autoimmunity (Leng et al., SLE study), and further drives monocyte and MDSC recruitment to the microenvironment and enhancing the expansion of M-MDSCs (Figure 6) (57, 60, 72, 73). This evidence concerns the gene CCL2 and Autoimmunity.