Under chronic exposure to interferon gamma (IFNγ), generated PMN-MDSCs also engage with macrophages to reprogram and polarize to peripheral alternatively activated macrophages which suppress the inflammation, promote tissue repair, remodeling, vasculogenesis, and retain homeostasis, via lessening CD40 expression and impairing IL-27 production, consequently facilitating immune evasion and causing dysfunctional myeloid responses in a SLE-prone model [16]. Here, IFNG is linked to systemic lupus erythematosus.