Figure 4.

DCs activate naive T cells by presenting antigens by phagocytosis, initiate immune responses, secrete chemotactic cytokines, chemotactic T/B cells, and present antigens to CD8 ⁺ T cells/CD4 ⁺ T cells by MHC class I/II cells. Upon activation of CD8 ⁺ T cells, perforin is released, and granzymes and FAS/FASL transmembrane glycoproteins kill tumors. mlDH1 inhibited the recruitment of CD8 ⁺ T cells and the expression of IFN-γ, whereas mlDH1 inhibitor could contact this inhibition. At the same time, HLA class I is expressed and presents tumor antigen-derived peptides to the immune system, which ultimately stimulate CD8 ⁺ T cells to show anti-tumor effects. Inhibition of B7-H4 by lentiviral transcription encoding shRNA could enhance CD8 ⁺ T cell-mediated cytotoxicity. The response of CD4 ⁺ T cells to mutated ERBB2IP antigen can be used to mediate the degeneration of metastatic epithelial cell carcinoma tissues, trametinib can lead to the up-regulation of MHC-I and PD-L1 on tumor cells in vitro, and the combination of trametinib with anti-PD-L1 drugs can enhance the anti-tumor toxicity of hepatic effector memory CD4 ⁺ T cells. The increased expression of TGF-β1 in tumor cells induces Tregs heterogeneity in TME, forms an environment conducive to tumor cell proliferation, anti-apoptosis and angiogenesis, and promotes tumor progression, a mechanism that can be inhibited by the combination of GCA. LAIR2 expressed by Tregs blocks the binding of LAIR1 by competing ligands, interferes with platelet activation and adhesion, and inhibits the classical pathway of the complement system and the lectin pathway to kill pathogens.