Figure 2.

Dendritic cells (DCs) play a pivotal role in the activation of naive T cells through the process of antigen presentation via phagocytosis. Moreover, they are responsible for initiating immune responses, secreting chemotactic cytokines to attract T/B cells, and presenting antigens to CD8⁺/CD4⁺ T cells via major histocompatibility complex class I/II (MHC I/II) cells. Upon activation of CD8⁺ T cells, the release of perforin, granzymes and Fas cell surface death receptor (FAS)/Fas ligand (FASL) transmembrane glycoproteins lead to the eradication of tumors. The recruitment of CD8⁺ T cells and the expression of interferon-gamma (IFN-γ) were found to be hindered by inhibiting mutant isocitrate dehydrogenase 1 (mIDH1). Simultaneously, the expression of human leukocyte antigen class I (HLA I) facilitates the presentation of tumor antigen-derived peptides to the immune system, thereby eliciting anti-tumor effects through the activation of CD8⁺ T cells. The application of lentiviral transcription encoding short hairpin RNA (shRNA) to inhibit B7 homolog 4 (B7H4) has the potential to enhance CD8⁺ T-cell-mediated cytotoxicity. The potential of CD4⁺ T cells to elicit a response against the mutated ERBB2 interacting protein (ERBB2IP) antigen holds promise for inducing degeneration in metastatic epithelial cell carcinoma tissues. In vitro studies have shown that trametinib can upregulate of MHC I and programmed cell death ligand-1 (PDL1) on tumor cells. Furthermore, the combination of trametinib with anti-PDL1 drugs can increase the anti-tumor activity of hepatic effector memory CD4⁺ T cells. The upregulation of transforming growth factor beta 1 (TGF-β1) in neoplastic cells induces heterogeneity in regulatory T cells (Tregs) within the TME, which forms a milieu for the proliferation of tumor cells, inhibits apoptosis, and stimulates angiogenesis. This process ultimately facilitates tumor progression, but can be counteracted by the concurrent administration of gemcitabine in combination with carboplatin. The expression of leukocyte-associated immunoglobulin-like receptor-2 (LAIR2) by Tregs hinders the binding of LAIR1 to competing ligands, disrupts platelet activation and adhesion, and impedes the classical pathway of the complement system and the lectin pathway. As a result, LAIR2 inhibits the elimination of pathogens. CTLs: cytotoxic T lymphocytes; PD1: programmed cell death protein-1; Th: T helper