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Fig. 1 | Molecular Cancer

Fig. 1

From: Prospects for chimeric antigen receptor-modified T cell therapy for solid tumors

Fig. 1

Immunosuppressive microenvironment in solid tumors. a Effector cells and target cells. Activated T cells often express some immune checkpoints that rapidly neutralize the antitumor activities, such as CTLA4, PD1, LAG3, TIM3, and VISTA, while the target cells express some immune checkpoint ligands, such as PDL1 or PDL2. In general, T cells lack some receptors, such as CCR2b or CCR4. In addition, CAR-T cell therapy is limited in solid tumors due to the paucity of tumor-specific antigens. b Immunosuppressive cells and cytokines. In the solid TEM, some immunosuppressive cells (e.g., Tregs, MDSCs, and TAMs) and released immunosuppressive cytokines (e.g., TGFβ and IL-10) significantly inhibit CAR-T cell cytotoxic function. c Physical barriers. Stroma-rich solid tumors have an abundance of ECM (e.g., HSPGs) that effectively inhibits the penetration and aggregation of T cells. d Intratumoral microenvironment. The intratumoral microenvironment is associated with hypoxia, nutrient starvation, and acidosis derived from elevated lactate generation. e Other immunosuppressive factors. CD47 allows tumor cells to evade immune surveillance mediated by CD47-SIRPα-mediated antiphagocytic signaling. Adenosine generated from extracellular AMP by the ectoenzyme CD73 results in unsuccessful application of CAR-T cell therapy. IDO contributes to tumor-induced tolerance through the degradation of tryptophan

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