Fig. 2
From: Targeting LAG-3, TIM-3, and TIGIT for cancer immunotherapy
The immunosuppression mechanisms underlying LAG-3 action in the TME. â‘ The interaction of LAG-3 and MHC-II between CD4 and tumor cells inhibits the proliferation and cytokine secretion of CD4 T cells, and the downstream MHC-II signal may support the survival of tumor cells. â‘¡ The interaction of LAG-3 and Galectin-3/LSECtin/FGL-1 between CTL/NK cells and the TME compartment inhibits the proliferation and cytotoxicity of CTL/NK cells. â‘¢ The interaction of LAG-3 and MHC-II between Tregs and tumor cells/DCs enhances the stability and immunosuppression capacity of Tregs. On the other hand, the maturation and immunostimulatory capacity of DCs are impaired by MHC-II downstream signaling. â‘£ The TME contains soluble LAG-3 (sLAG-3), which can impair the antigen-presenting function of monocyte-derived DCs (mDCs) or even inhibit the differentiation of monocytes into DCs