Fig. 1
From: The role of DNA damage repair (DDR) system in response to immune checkpoint inhibitor (ICI) therapy
DDR pathway disorders contribute to immune recognition and tumor killing by increasing tumor immunogenicity. DDR mutation/inhibition impedes damaged DNA repair, enlarges chromosomal variation, and thus increases the levels of the tumor mutational burden (TMB) and neoantigen load (NAL). This subsequently activates CTLs and NK cells to exert anti-tumor activity via upregulating MHC-I and the antigen presentation process of APCs. This includes DCs and TAMs. At the same time, more tumor infiltrating lymphocytes (TILs) are recruited. (APC: Antigen-presenting cell; CTL: Cytotoxic T lymphocyte; DC: Dendritic cell; DDR: DNA damage repair; DSB: DNA double strand break; GZMA: Granzyme A; IL-2: Interleukin-2; NK cells: Natural killer cells; PRF1: Perforin 1; SSB: DNA single strand break; TAM: Tumor-associated macrophage)