Fig. 1

The initiation and regulation of antitumor immunity in EC. EC cells harbor abundant tumor antigens and are able to induce antitumor immune response, particularly in the early stage of EC. However, during tumor development, EC cells acquire the ability to escape immune surveillance through various ways. EC esophageal cancer, NKG2D natural killer group 2D, IL-12 interleukin-12, IFN-γ interferon-γ, MHC-I major histocompatibility complex class I, MHC-II major histocompatibility complex class II, IL-6 interleukin-6, TGF-β transforming growth factor-β, IL-10 interleukin-10, PD-L1/2 programmed death-ligand 1/2, PD-1 programmed cell death protein 1, TIM-3 T-cell immunoglobulin and mucin-domain containing-3, CTLA-4 cytotoxic T lymphocyte-associated protein 4, LAG-3, lymphocyte-activation gene 3, IDO1 indoleamine 2,3-dioxygenase 1, ROS reactive oxygen species, i-NOS inducible nitric oxide synthase, Arg-1 Arginase-1, NK natural killer, Th1 type 1 T helper, cDC1 conventional type 1 dendritic cell, CAF cancer-associated fibroblast, Treg regulatory T cell, TAM tumor-associated macrophage, MDSC myeloid-derived suppressor cell