Robert, C. et al. Pembrolizumab versus ipilimumab in advanced melanoma. N. Engl. J. Med. 372, 2521–2532 (2015).

Article  CAS  PubMed  Google Scholar 

Hodi, F. S. et al. Improved survival with ipilimumab in patients with metastatic melanoma. N. Engl. J. Med. 363, 711–723 (2010).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Brahmer, J. et al. Nivolumab versus docetaxel in advanced squamous-cell non-small-cell lung cancer. N. Engl. J. Med. 373, 123–135 (2015).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Herbst, R. S. et al. Atezolizumab for first-line treatment of PD-L1-selected patients with NSCLC. N. Engl. J. Med. 383, 1328–1339 (2020).

Article  CAS  PubMed  Google Scholar 

Bellmunt, J. et al. Pembrolizumab as second-line therapy for advanced urothelial carcinoma. N. Engl. J. Med. 376, 1015–1026 (2017).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Ahmadzadeh, M. et al. Tumor antigen-specific CD8 T cells infiltrating the tumor express high levels of PD-1 and are functionally impaired. Blood 114, 1537–1544 (2009).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Curiel, T. J. et al. Blockade of B7-H1 improves myeloid dendritic cell-mediated antitumor immunity. Nat. Med. 9, 562–567 (2003).

Article  CAS  PubMed  Google Scholar 

O’Malley, G. et al. Stromal cell PD-L1 inhibits CD8+ T-cell antitumor immune responses and promotes colon cancer. Cancer Immunol. Res. 6, 1426–1441 (2018).

Article  CAS  PubMed  Google Scholar 

Krummel, M. F. & Allison, J. P. CD28 and CTLA-4 have opposing effects on the response of T cells to stimulation. J. Exp. Med. 182, 459–465 (1995).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Wei, S. C. et al. Distinct cellular mechanisms underlie anti-CTLA-4 and anti-PD-1 checkpoint blockade. Cell 170, 1120–1133.e1117 (2017).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Simpson, T. R. et al. Fc-dependent depletion of tumor-infiltrating regulatory T cells co-defines the efficacy of anti-CTLA-4 therapy against melanoma. J. Exp. Med. 210, 1695–1710 (2013).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Wu, R. et al. A functional variant at miR-132-3p, miR-212-3p, and miR-361-5p binding site in CD80 gene alters susceptibility to gastric cancer in a Chinese Han population. Med. Oncol. 31, 60 (2014).

Article  PubMed  Google Scholar 

Wu, D. et al. Five functional polymorphisms of B7/CD28 co-signaling molecules alter susceptibility to colorectal cancer. Cell Immunol. 293, 41–48 (2015).

Article  CAS  PubMed  Google Scholar 

Wang, W. et al. A miR-570 binding site polymorphism in the B7-H1 gene is associated with the risk of gastric adenocarcinoma. Hum. Genet. 132, 641–648 (2013).

Article  CAS  PubMed  Google Scholar 

Sun, T. et al. Functional genetic variations in cytotoxic T-lymphocyte antigen 4 and susceptibility to multiple types of cancer. Cancer Res. 68, 7025–7034 (2008).

Article  CAS  PubMed  Google Scholar 

Kataoka, K. et al. Integrated molecular analysis of adult T cell leukemia/lymphoma. Nat. Genet. 47, 1304–1315 (2015).

Article  CAS  PubMed  Google Scholar 

Georgiou, K. et al. Genetic basis of PD-L1 overexpression in diffuse large B-cell lymphomas. Blood 127, 3026–3034 (2016).

Article  CAS  PubMed  Google Scholar 

The Cancer Genome Atlas Research Network. Comprehensive molecular characterization of gastric adenocarcinoma. Nature 513, 202–209 (2014).

Article  Google Scholar 

Stein, A. et al. PD-L1 targeting and subclonal immune escape mediated by PD-L1 mutations in metastatic colorectal cancer. J. Immunother. Cancer https://doi.org/10.1136/jitc-2021-002844 (2021).

Article  PubMed  PubMed Central  Google Scholar 

Claass, L. V. et al. PD-L1 amino acid position 88 represents a hotspot for PD-L1 stability with relevance for PD-L1 inhibition. Front. Oncol. 12, 941666 (2022).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Wang, W. et al. A frequent somatic mutation in CD274 3′-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding. Hum. Mutat. 33, 480–484 (2012).

Article  CAS  PubMed  Google Scholar 

Twa, D. D. et al. Genomic rearrangements involving programmed death ligands are recurrent in primary mediastinal large B-cell lymphoma. Blood 123, 2062–2065 (2014).

Article  CAS  PubMed  Google Scholar 

Green, M. R. et al. Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma. Blood 116, 3268–3277 (2010).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Kataoka, K. et al. Aberrant PD-L1 expression through 3′-UTR disruption in multiple cancers. Nature 534, 402–406 (2016). Seminal discovery that structural variants disrupting the 3′-UTR of CD274 lead to constitutive overexpression and immune evasion in multiple cancer types.

Article  CAS  PubMed  Google Scholar 

Steidl, C. et al. MHC class II transactivator CIITA is a recurrent gene fusion partner in lymphoid cancers. Nature 471, 377–381 (2011).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Chapuy, B. et al. Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes. Nat. Med. 24, 679–690 (2018).

Article  CAS  PubMed  PubMed Central  Google Scholar 

Majzner, R. G. et al. CD58 aberrations limit durable responses to CD19 CAR in large B cell lymphoma patients treated with axicabtagene ciloleucel but can be overcome through novel CAR engineering. Blood 136, 53–54 (2020).

Article  Google Scholar 

Xu, X. et al. CD58 genetic alterations and its contribution to upregulation of PD-L1 and IDO via LYN/CD22/SHP1 axis in DLBCL. Blood 142, 524 (2023).

Article  Google Scholar 

Miao, B. et al. CMTM6 shapes antitumor T cell response through modulating protein expression of CD58 and PD-L1. Cancer Cell 41, 1817–1828.e1819 (2023). This study, and Ho et al., are key studies demonstrating how co-stimulatory and inhibitory checkpoint axes are coordinately regulated through shared post-translational mechanisms.

Article  CAS  PubMed  PubMed Central  Google Scholar 

Ho, P. et al. The CD58-CD2 axis is co-regulated with PD-L1 via CMTM6 and shapes anti-tumor immunity. Cancer Cell 41, 1207–1221.e1212 (2023). This study, and Miao et al., are key studies demonstrating how co-stimulatory and inhibitory checkpoint axes are coordinately regulated through shared post-translational mechanisms.

Article  CAS  PubMed  PubMed Central  Google Scholar 

Yan, X. et al. CD58 loss in tumor cells confers functional impairment of CAR T cells. Blood Adv. 6, 5844–5856 (2022).

Article  CAS  PubMed