The DOI matches its Crossref record; 134 of the 134 references it cites were found in a registry or an index.
IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression
Open accessAbstract
Aryl hydrocarbon receptor (AHR) activation by tryptophan (Trp) catabolites enhances tumor malignancy and suppresses anti-tumor immunity. The context specificity of AHR target genes has so far impeded systematic investigation of AHR activity and its upstream enzymes across human cancers. A pan-tissue AHR signature, derived by natural language processing, revealed that across 32 tumor entities, interleukin-4-induced-1 (IL4I1) associates more frequently with AHR activity than IDO1 or TDO2, hitherto recognized as the main Trp-catabolic enzymes. IL4I1 activates the AHR through the generation of indole metabolites and kynurenic acid. It associates with reduced survival in glioma patients, promotes cancer cell motility, and suppresses adaptive immunity, thereby enhancing the progression of chronic lymphocytic leukemia (CLL) in mice. Immune checkpoint blockade (ICB) induces IDO1 and IL4I1. As IDO1 inhibitors do not block IL4I1, IL4I1 may explain the failure of clinical studies combining ICB with IDO1 inhibition. Taken together, IL4I1 blockade opens new avenues for cancer therapy.
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Cited by
Tryptophan metabolism in health and disease
Xue, C., Li, G., Zheng, Q., Gu, X., Shi, Q., Su, Y., Chu, Q., Yuan, X., Bao, Z., Lu, J., et al. (2023) · Cell Metabolism · doi:10.1016/j.cmet.2023.06.004 · Cited by 961
Macrophage diversity in cancer revisited in the era of single-cell omics
Ma, R.-Y., Black, A., & Qian, B.-Z. (2022) · Trends in Immunology · doi:10.1016/j.it.2022.04.008 · Cited by 698
Cross-tissue single-cell landscape of human monocytes and macrophages in health and disease
Mulder, K., Patel, A. A., Kong, W. T., Piot, C., Halitzki, E., Dunsmore, G., Khalilnezhad, S., Irac, S. E., Dubuisson, A., Chevrier, M., et al. (2021) · Immunity · doi:10.1016/j.immuni.2021.07.007 · Cited by 678
Immune checkpoint therapy for solid tumours: clinical dilemmas and future trends
Sun, Q., Hong, Z., Zhang, C., Wang, L., Han, Z., & Ma, D. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01522-4 · Cited by 598
Indoleamine 2,3-dioxygenase (IDO) inhibitors and cancer immunotherapy
Fujiwara, Y., Kato, S., Nesline, M. K., Conroy, J. M., DePietro, P., Pabla, S., & Kurzrock, R. (2022) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2022.102461 · Cited by 304
Metadata
- Authors
- Sadik, A., Somarribas Patterson, L. F., Öztürk, S., Mohapatra, S. R., Panitz, V., Secker, P. F., Pfänder, P., Loth, S., Salem, H., Prentzell, M. T., Berdel, B., Iskar, M., Faessler, E., Reuter, F., Kirst, I., Kalter, V., Foerster, K. I., Jäger, E., Guevara, C. R., Sobeh, M., Hielscher, T., Poschet, G., Reinhardt, A., Hassel, J. C., Zapatka, M., Hahn, U., von Deimling, A., Hopf, C., Schlichting, R., Escher, B. I., Burhenne, J., Haefeli, W. E., Ishaque, N., Böhme, A., Schäuble, S., Thedieck, K., Trump, S., Seiffert, M., & Opitz, C. A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-09
- Volume
- 182
- Issue
- 5
- Pages
- 1252-1270.e34
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W3049896770
- Cited by
- 559
- References
- 134
- FWCI
- 20.69
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Sadik, A., Somarribas Patterson, L. F., Öztürk, S., Mohapatra, S. R., Panitz, V., Secker, P. F., Pfänder, P., Loth, S., Salem, H., Prentzell, M. T., Berdel, B., Iskar, M., Faessler, E., Reuter, F., Kirst, I., Kalter, V., Foerster, K. I., Jäger, E., Guevara, C. R., . . . Opitz, C. A. (2020). IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression. Cell. https://doi.org/10.1016/j.cell.2020.07.038
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
