Overcoming Genetically Based Resistance Mechanisms to PD-1 Blockade
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Abstract
Mechanism-based strategies to overcome resistance to PD-1 blockade therapy are urgently needed. We developed genetic acquired resistant models of JAK1, JAK2, and B2M loss-of-function mutations by gene knockout in human and murine cell lines. Human melanoma cell lines with JAK1/2 knockout became insensitive to IFN-induced antitumor effects, while B2M knockout was no longer recognized by antigen-specific T cells and hence was resistant to cytotoxicity. All of these mutations led to resistance to anti–PD-1 therapy in vivo. JAK1/2-knockout resistance could be overcome with the activation of innate and adaptive immunity by intratumoral Toll-like receptor 9 agonist administration together with anti–PD-1, mediated by natural killer (NK) and CD8 T cells. B2M-knockout resistance could be overcome by NK-cell and CD4 T-cell activation using the CD122 preferential IL2 agonist bempegaldesleukin. Therefore, mechanistically designed combination therapies can overcome genetic resistance to PD-1 blockade therapy. Significance: The activation of IFN signaling through pattern recognition receptors and the stimulation of NK cells overcome genetic mechanisms of resistance to PD-1 blockade therapy mediated through deficient IFN receptor and antigen presentation pathways. These approaches are being tested in the clinic to improve the antitumor activity of PD-1 blockade therapy. This article is highlighted in the In This Issue feature, p. 1079
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JAK1/2-inactivating mutations reduce PD-L1 and MHC I expression in mouse and human CRC.
“JAK1/2-inactivating mutations reduce programmed death ligand 1 (PD-L1) and MHC I expression in mouse and human CRC [33,210].”
From Drug Resistance in Colorectal Cancer: From Mechanism to Clinic (2022) · cites this paper as [33]
Inactivation mutations of JAK1 and JAK2 block the IFN-γ signaling pathway, leading to downregulation of tumor PD-L1 expression, so anti-PD-L1 therapy would be unnecessary in this case.
“This implies that the inactivation mutations of JAK1 and JAK2 block the IFN-γ signaling pathway, leading to downregulation of tumor PD-L1 expression, so it would be unnecessary to attempt anti-PD-L1 therapy in this case.”
From Drug Resistance in Colorectal Cancer: From Mechanism to Clinic (2022) · cites this paper as [33]
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Orsini, A., Diquigiovanni, C., & Bonora, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241612690 · Cited by 52 · see citing works
- Authors
- Torrejon, D. Y., Abril-Rodriguez, G., Champhekar, A. S., Tsoi, J., Campbell, K. M., Kalbasi, A., Parisi, G., Zaretsky, J. M., Garcia-Diaz, A., Puig-Saus, C., Cheung-Lau, G., Wohlwender, T., Krystofinski, P., Vega-Crespo, A., Lee, C. M., Mascaro, P., Grasso, C. S., Berent-Maoz, B., Comin-Anduix, B., Hu-Lieskovan, S., & Ribas, A.
- Affiliations
- University of California, Los Angeles (US)
- 1Division of Hematology-Oncology, Department of Medicine, University of California, Los Angeles, Los Angeles, California.
- 4Division of Surgical Oncology, Department of Surgery, University of California, Los Angeles, Los Angeles, California.
- Corresponding author
- Ribas, Antoni
- ORCID
- Venue
- Cancer Discovery
- Published
- 2020-08-01
- Volume
- 10
- Issue
- 8
- Pages
- 1140-1157
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC7416458
- OpenAlex
- W3030418407
- Cited by
- 146
- References
- 75
- Citations by year
- 2026: 18 · 2025: 16 · 2024: 26 · 2023: 31 · 2022: 26 · 2021: 25 · 2020: 4
- FWCI
- 7.77
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- NIH (R35 CA197633, P01 CA244118, #T32-CA009120, GM08042, P30 CA016042, 5P30 AI028697)
- UCLA (T32CA009120)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- anti-PD-1 therapy, immune checkpoint inhibitor resistance, B2M knockout, interferon signaling, melanoma, Toll-like receptor 9 agonist, natural killer cells, CD8+ T cells, CD4+ T cells, interleukin-2, combination immunotherapy, gene knockout models
- MeSH terms
- Loss of Function Mutation, Animals, beta 2-Microglobulin, Humans, Interferons, Interleukin-2, Killer Cells, Natural, Mice, Inbred C57BL, Neoplasms, Polyethylene Glycols, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Drug Resistance, Neoplasm, Cell Line, Tumor, Cell Proliferation, Toll-Like Receptor 9, Janus Kinase 1, Janus Kinase 2, Programmed Cell Death 1 Receptor
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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