ArticleOncotarget2017
Restoration of immune surface molecules in Kaposi sarcoma-associated herpes virus infected cells by lenalidomide and pomalidomide.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Safety, Activity, and Long-term Outcomes of Pomalidomide in the Treatment of Kaposi Sarcoma among Individuals with or without HIV Infection.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- Caspase cleavage of Kaposi sarcoma-associated herpesvirus proteins: a role for K5 in preventing caspase-mediated cell death during lytic replication.Journal of virology · 2025Article
- Novel Cereblon-Binding Immunomodulators Have Increased Potency Against Gammaherpesvirus- Associated Lymphomas In Vitro.Journal of medical virology · 2025Article
- Primary Effusion Lymphoma Prognostic Score (PEL-PS): A Validated International Prognostic Score in HIV-Associated Primary Effusion Lymphoma.American journal of hematology · 2025Article
- Modern Approach to Manage Patients With Kaposi Sarcoma.Journal of medical virology · 2025Review
- Review
- Review
- Hypoxic reactivation of Kaposi's sarcoma associated herpesvirus.Cell insight · 2024Review
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- The interplay between persistent pathogen infections with tumor microenvironment and immunotherapy in cancer.Cancer medicine · 2024Review
- Promising immunotherapeutic approaches for primary effusion lymphoma.Exploration of targeted anti-tumor therapy · 2024Review
- Article
- Mechanism and therapeutic implications of pomalidomide-induced immune surface marker upregulation in EBV-positive lymphomas.Scientific reports · 2023Article
- Today's Kaposi sarcoma is not the same as it was 40 years ago, or is it?Journal of medical virology · 2023Review
- Daratumumab induces cell-mediated cytotoxicity of primary effusion lymphoma and is active against refractory disease.Oncoimmunology · 2023Article
- The role of viruses in HIV-associated lymphomas.Seminars in hematology · 2022Article
- Immunotherapy for KSHV-associated diseases.Current opinion in virology · 2022Review
- CDK4/6 inhibitors sensitize gammaherpesvirus-infected tumor cells to T-cell killing by enhancing expression of immune surface molecules.Journal of translational medicine · 2022Article
- KSHV/HHV8-mediated hematologic diseases.Blood · 2022Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi sarcoma-associated herpesvirus (KSHV) is the cause of several tumors, including Kaposi sarcoma and primary effusion lymphoma (PEL). Most viruses have evolved means of escaping immune recognition. KSHV downregulates MHC-I expression during lytic infection, and expression of ICAM-1 and B7-2 (CD86) during latent infection, allowing evasion of T cell and natural killer immunity respectively. These effects are largely mediated by two KSHV-encoded proteins, K3 and K5. We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells. Importantly, these changes occurred at clinically achievable concentrations and prior to any cytotoxic effects. Exploration of the mechanism revealed that Pom blocked lytic down-regulation of MHC-I induced by transfection with K3 but not K5. Although Pom alone did not significantly increase HLA mRNA expression in PEL cells, it did blunt the butyrate-induced decrease in MHC-I mRNA expression and decreased the upregulation of K3 mRNA in lytic cells. Virus-induced tumors express foreign antigens, but immunotherapy can be thwarted by viral strategies to evade immune recognition. The effects of Pom and Len described here can prevent these strategies and support the use of these drugs to treat KSHV-induced tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.