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Summary
| Description |
English: Figure 4 KEAP1/NRF2 modulation of antitumor immune responses. (a) Lung cancer patients with KEAP1-mutant tumors display signs of immune evasion with the exclusion of T cells. NRF2 activation by KEAP1 mutation may be selected for in lung cancer by enabling tumors to overcome metabolic bottlenecks [e.g., ROS (reactive oxygen species), hypoxia, nutrient availability] and suppress antitumor immune responses by altering the immune composition (e.g., T cells, myeloid cells, or other immune cell populations). Panel adapted with permission from Sayin et al. (2019). (b) Potential interactions of KEAP1-mutant cells with immune cell populations in the tumor microenvironment (TME). Metabolites secreted [e.g., lactate, GSH (glutathione)] or consumed (e.g., glucose, amino acids) by KEAP1-mutant tumors may alter the metabolic composition of the TME, therefore impacting the activity and function of effector T cells. In addition to a potential metabolism-dependent immune suppression, NRF2 transcriptionally regulates immunomodulatory pathways such as chemokines/cytokines (e.g., IL-1, -6, -11, -17d) and cGAS/STING-induced type I interferon (IFN). |
| Date | |
| Source | https://www.annualreviews.org/doi/full/10.1146/annurev-cancerbio-030518-055627 |
| Author | Warren L. Wu and Thales Papagiannakopoulos |
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| Date/Time | Thumbnail | Dimensions | User | Comment | |
|---|---|---|---|---|---|
| current | 21:21, 12 September 2020 | | 2,791 × 3,869 (954 KB) | Elysia (AR) | Uploaded a work by Warren L. Wu and Thales Papagiannakopoulos from https://www.annualreviews.org/doi/full/10.1146/annurev-cancerbio-030518-055627 with UploadWizard |
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