Figure 5.

Proposed mechanism of LILRB-mediated immune-evasion and tumour progression via myeloid cells. Engagement of LILRB1 and LILRB2 with HLA-G on myeloid-derived suppressor cells (MDSC) activates STAT6 and STAT3-mediated cascades, which in turn induces ARG1 and IDO production responsible for T cell suppression. LILRB4 ligation by APOE on monocytic AML cells mediates SHP-2 inhibitory signalling, which in turn positively regulate the NF-κB pathway. This leads to ARG1 production and urokinase-type plasminogen activator receptor (uPAR), responsible for T cell suppression and support of leukaemia migration. Although further studies are needed, LILRB3 ligation can mediate similar processes, such as induction of amphiregulin.