T cell effects and mechanisms in immunotherapy of head and neck tumors

Abstract

Head and neck tumors (HNCs) are a common tumor in otorhinolaryngology head and neck surgery, accounting for 5% of all malignant tumors in the body and are the sixth most common malignant tumor worldwide. In the body, immune cells can recognize, kill, and remove HNCs. T cell-mediated antitumor immune activity is the most important antitumor response in the body. T cells have different effects on tumor cells, among which cytotoxic T cells and helper T cells play a major killing and regulating role. T cells recognize tumor cells, activate themselves, differentiate into effector cells, and activate other mechanisms to induce antitumor effects. In this review, the immune effects and antitumor mechanisms mediated by T cells are systematically described from the perspective of immunology, and the application of new immunotherapy methods related to T cells are discussed, with the objective of providing a theoretical basis for exploring and forming new antitumor treatment strategies. Video Abstract.

Keywords: Head and neck cancer; Immune checkpoint inhibitor (ICI); Immunotherapy; Major histocompatibility complex (MHC).

Fig. 1

HNCs can inhibit t-cell-mediated activation of immune responses through three pathways. 1 Tumor cells can express MHC I molecules on the cell surface and form an antigenic peptide-MHC CLASS I molecular complex through the MHC I pathway, which provides the first signal for T cell activation. CD8+ T cells can initially transform into CTL after receiving the first signal 2 At the same time, tumor cells can recognize MHC class II molecules on the surface of APC cells by pattern recognition receptors (PRR). Some MHC II molecules can form the first signal through cross-presentation and participate in the initial activation of CTL cells through the endogenous antigen presentation pathway. Other MHC CLASS II molecules can form an antigenic peptide-MHC Class II molecular complex through the MHC II pathway to activate CD4+ T cells to produce costimulatory molecules, and at the same time provide a second signal for the activation of CD8+ T cells to fully activate and maintain CTL proliferation and cloning. 3 Tumor cells and APC cells can also secrete costimulatory molecules and participate in the formation of the secondary signal

Fig. 2

a Tumor cells express MHC-I molecules to provide the first signal for T cell activation through the MHC-I pathway, leading to initial activation of CD8+ T cells in CTL. b The APC recognizes tumor cells using pattern recognition receptors (PRRs), and then expresses MHC-II molecules and delivers them to CD4+ T cells, activating Th cells. c DCs can cross-present MHC-II molecules to CD8+ T cells through the MHC-I pathway and induce their differentiation into CTL. d APC and Th cells can produce a variety of co-stimulatory molecules, which provide a second signal for T cell activation, which allows T cells to fully activate