MYD88 and skin infection: Furthermore, TLR activation by S. aureus lipoproteins can result in MDSC expansion and can regulate MDSC functioning; during an S. aureus skin infection, resident skin cells were stimulated to secrete IL-6 by TLR2 activation, which resulted in recruitment and accumulation of MDSCs [13], while TLRs regulate the immunosuppressive function of MDSCs via the upregulation of iNOS and Arg-1 through MyD88 and NF-κB signaling [11].