ArticleInternational immunology2022
Cancer-derived cholesterol sulfate is a key mediator to prevent tumor infiltration by effector T cells.
Article in International immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Early-stage drug discovery in a new-generation ultrahigh-throughput mass spectrometry platform.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- High-Content SRS Imaging Unveils Altered Cholesterol Metabolism in Ovarian Cancers Under CAR-T Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Review
- Sulfotransferase SULT2B1 contributes to the epithelial-immune microenvironment homeostasis in imiquimod-induced psoriatic dermatitis.Frontiers in immunology · 2025Article
- Metabolic gatekeepers: harnessing tumor-derived metabolites to optimize T cell-based immunotherapy efficacy in the tumor microenvironment.Cell death & disease · 2024Review
- Article
- A new type of sulfation reaction:PNAS nexus · 2024Article
- Human sulfotransferaseFrontiers in genetics · 2024Review
- Metabolomic profile of acute myeloid leukaemia parallels of prognosis and response to therapy.Scientific reports · 2023Article
- The Immunosuppressive Potential of Cholesterol Sulfate Through T Cell Microvilli Disruption.Immune network · 2023Article
- Sulfotransferase 2B1b, Sterol Sulfonation, and Disease.Pharmacological reviews · 2023Review
- Tumor-intrinsic metabolic reprogramming and how it drives resistance to anti-PD-1/PD-L1 treatment.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Cholesterol sulfate limits neutrophil recruitment and gut inflammation during mucosal injury.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effective tumor immunotherapy requires physical contact of T cells with cancer cells. However, tumors often constitute a specialized microenvironment that excludes T cells from the vicinity of cancer cells, and its underlying mechanisms are still poorly understood. DOCK2 is a Rac activator critical for migration and activation of lymphocytes. We herein show that cancer-derived cholesterol sulfate (CS), a lipid product of the sulfotransferase SULT2B1b, acts as a DOCK2 inhibitor and prevents tumor infiltration by effector T cells. Using clinical samples, we found that CS was abundantly produced in certain types of human cancers such as colon cancers. Functionally, CS-producing cancer cells exhibited resistance to cancer-specific T-cell transfer and immune checkpoint blockade. Although SULT2B1b is known to sulfate oxysterols and inactivate their tumor-promoting activity, the expression levels of cholesterol hydroxylases, which mediate oxysterol production, are low in SULT2B1b-expressing cancers. Therefore, SULT2B1b inhibition could be a therapeutic strategy to disrupt tumor immune evasion in oxysterol-non-producing cancers. Thus, our findings define a previously unknown mechanism for tumor immune evasion and provide a novel insight into the development of effective immunotherapies.
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