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. 2021 Dec 23;12:773168. doi: 10.3389/fimmu.2021.773168

Figure 1.

Figure 1

The cross talk between immune cells in TME and the role of immune cells in the efficacy of PD-1 inhibitor therapy. CD8+T cells recognize antigens requiring a corroboration work between CD4+T cells with NK cells and DCs, and M1 TAM can exert antitumoral effects due to the stimulation of IFN-γ produced by CD8+ T cells. In addition to these immunostimulatory cells, the immunoinhibitory cells including CAFs, Tregs, M2 TAMs, and MDSCs can construct an immunosuppressive microenvironment to restrict the antitumor effect. Anti-PD-1 binds to PD-1 on immune cells which can block PD-1/PD-L1 interactions and recover the antitumor function of those cells. PD-1, programmed cell death protein 1; PD-L1, programmed death-ligand 1; PD-L2, programmed death-ligand 2; IFN-γ, interferon gamma; TNF, tumor necrosis factor; CTL, cytotoxic T lymphocyte; DC, dendritic cell; NK, natural killer cell; MDSC, myeloid-derived suppressor cell; Treg, regulatory T cell; CAF, cancer-associated fibroblast; TAM, tumor-associated macrophage; M1, type 1 macrophage cell; M2, type 2 macrophage cell; MHC, major histocompatibility complex; TCR, T cell receptor; TME, tumor microenvironment.