Integrin αvβ8 on T cells is responsible for suppression of anti-tumor immunity in multiple syngeneic models and is a promising target for tumor immunotherapy
Open accessAbstract
The αvβ8 integrin is a key activator of transforming growth factor β (TGF β), which has been shown to inhibit anti-tumor immunity. Previous work has suggested that αvβ8 on tumor cells could modulate tumor growth and responses to immune checkpoint blockade. We now show that a potent blocking monoclonal antibody against αvβ8 (ADWA-11) causes growth suppression or complete regression in syngeneic models of squamous cell carcinoma (CCK168), mammary cancer (EMT-6), colon cancer (CT26), and prostate cancer (TRAMPC2), especially when it is combined with other immunomodulators (anti-PD-1, anti-CTLA-4 or 4-1BB) or radiotherapy. αvβ8 is expressed on tumor cells in some of these models, but tumor cell expression of αvβ8 is not essential for the beneficial effects of ADWA-11 therapy. αvβ8 is consistently expressed at highest levels on CD4+CD25+ T cells within tumors, and specific deletion of Itgb8 from T cells is as effective as ADWA-11 in suppressing tumor growth. Treatment with ADWA-11 increases expression of a suite of genes in tumor infiltrating CD8+ T cells that are normally inhibited by TGFβ and are involved in tumor cell killing, including Granzyme B and Interferon-γ. These findings solidify αvβ8 integrin as a promising target for cancer immunotherapy, even for tumors that do not express this integrin.
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Success of classical cancer therapies is based on early regression of the primary tumor, using RECIST, which commonly results from direct cytotoxic effects on cancer cells.
“Success of classical cancer therapies, i.e. chemotherapy, radiation and molecular targeted therapies, is based on early regression of the primary tumor, using Response Evaluation Criteria In Solid Tumors, or RECIST321, which commonly results from direct cytotoxic effects on cancer cells.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [321]
Immunotherapy, including TGF-β blockade, does not routinely result in short-term endpoints assessed by RECIST.
“In contrast to chemotherapy or oncogene-targeted drugs, immunotherapy, including TGF-β blockade, does not routinely result in short-term endpoints that are assessed by RECIST321.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [321]
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- Authors
- Dodagatta-Marri, E., Ma, H.-Y., Liang, B., Li, J., Meyer, D. S., Sun, K.-H., Ren, X., Zivak, B., Rosenblum, M. D., Headley, M. B., Pinzas, L., Reed, N. I., Del Cid, J. S., Adoumie, M., Hann, B. C., Yang, S., Giddabasappa, A., Noorbehesht, K., Yang, B., Dal Porto, J., Tsukui, T., Niessen, K., Atakilit, A., Akhurst, R. J., & Sheppard, D.
- Affiliations
- University of California, San Francisco (US)
- Shandong University (CN)
- Pfizer (United States) (US)
- Corresponding author
- Akhurst, Rosemary J.
- Sheppard, Dean
- ORCID
- Venue
- Cell Reports
- Publisher
- openRxiv
- Published
- 2020-05-15
- Volume
- 36
- Issue
- 1
- Pages
- 109309-109309
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC8321414
- OpenAlex
- W3178899807
- Cited by
- 70
- References
- 38
- Citations by year
- 2026: 11 · 2025: 15 · 2024: 11 · 2023: 16 · 2022: 7 · 2021: 9 · 2020: 1
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Pfizer
- National Institutes of Health
- University of California, San Francisco
- National Heart, Lung, and Blood Institute (K08HL111208, KHL111208A)
- National Cancer Institute (R01CA197198, R01CA210561, U01CA217864, P30CA082103, R01CA197363)
- Comprehensive Transplant Institute, University of Alabama at Birmingham
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- integrin αvβ8, TGF-beta signaling, tumor immunosuppression, CD4+CD25+ T cells, CD8+ T cell cytotoxicity, tumor-infiltrating lymphocytes, granzyme B, interferon-gamma, cancer immunotherapy, squamous cell carcinoma, breast cancer, colon cancer, prostate cancer, combined radiotherapy
- MeSH terms
- Animals, Antibodies, Neoplasm, Immunity, Immunotherapy, Interferon-gamma, Lymphocyte Depletion, Male, Mice, Inbred C57BL, Mice, Transgenic, Models, Biological, Mutation, Neoplasms, T-Lymphocytes, T-Lymphocytes, Cytotoxic, Signal Transduction, CD4-Positive T-Lymphocytes, Gene Expression Regulation, Neoplastic, Survival Analysis, Integrins, Transforming Growth Factor beta, CD8-Positive T-Lymphocytes, Cell Line, Tumor, Cell Proliferation, Mice, Smad3 Protein, Tumor Necrosis Factor Receptor Superfamily, Member 9, Granzymes, Tumor Microenvironment, CTLA-4 Antigen
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