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. 2022 Dec 23;15(1):104. doi: 10.3390/cancers15010104

Figure 4.

Figure 4

T cell exhaustion contributes to therapeutic resistance of TNBC to PD-1/PD-L1 inhibitors. Continuous exposure of T cells to tumor antigens and suppressive cytokines (IL-10, TGF-β) leads to T cell exhaustion, which results in a poor response to immunotherapy and therapeutic resistance. The accumulated ROS, increased HIF-α and activated calcium-calcineurin-NFAT signaling pathway play a key role in T cell exhaustion, which contributes to therapeutic resistance. Abbreviations: PD-1, programmed cell death protein 1; PD-L1, programmed cell death 1 ligand 1; TCR, T cell receptor; MHC, major histocompatibility complex; APC, antigen-presenting cell; TNBC, triple negative breast cancer; TIM-3, T cell immunoglobulin domain and mucin domain-3; TGF-β, transforming growth factor-beta; IL-10, interleukin-10; IL-1, interleukin-1; IFN-γ, interferon-γ; TNF-α, tumor necrosis factor-α; ROS, reactive oxygen species; NFAT, nuclear factor of activated T cells; HIF-1α, hypoxia inducible factor-1α; TOX, thymocyte selection associated high mobility group box; BATF, basic leucine zipper transcriptional factor ATF-like; IFR-4, interferon regulatory factor 4.