Figure 1.

Cellular and humoral immune responses induced by hTERT. The hTERT protein produced by cancer cells binds to MHC class I molecules in tumor cells to form antigenic peptide-MHC class I molecule complexes that are presented on the cell surface. CTLs recognize and bind to these complexes and subsequently release perforin, granzyme, cytokines, etc. to kill cancer cells. Following cell death by apoptosis or necrosis, cancer cells release tumor antigens that are phagocytosed by APCs (including DCs and B lymphocytes). APCs present antigenic peptides (derived from hTERT)-MHC class I or II complexes to CD8⁺ T cells and CD4⁺ T cells, respectively. Activated CD8⁺ T cells differentiate into CTLs and proliferate; these cells are recruited to the tumor site and further kill cancer cells. In contrast, CD4⁺ T cells can differentiate into various types of Th cells and release various cytokines to help activate CD8⁺ T cells and B cells and enhance the killing activity of CTLs. B cells are activated into plasmocyte under the combined action of antigenic peptides and Th cells, and plasmocytes synthesize and secrete a large number of antibodies to exert antitumor effect. TCR, T cell receptor; MHC, major histocompatibility complex; APC, antigen-presenting cell; CTL, cytotoxic T lymphocyte; BCR, B cell receptor; hTERT, human telomerase reverse transcriptase; DC, dendritic cell.