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Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells
Most chronic viruses evade T-cell and natural killer (NK) immunity through downregulation of immune surface markers. Previously we showed that Pomalidomide (Pom) increases surface expression of major histocompatibility complex class I (MHC-I) in Kaposi sarcoma-associated herpesvirus-infected latent...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343774/ https://www.ncbi.nlm.nih.gov/pubmed/30713808 http://dx.doi.org/10.1080/2162402X.2018.1546544 |
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author | Davis, David A. Shrestha, Prabha Aisabor, Ashley I. Stream, Alexandra Galli, Veronica Pise-Masison, Cynthia A. Tagawa, Takanobu Ziegelbauer, Joseph M. Franchini, Genoveffa Yarchoan, Robert |
author_facet | Davis, David A. Shrestha, Prabha Aisabor, Ashley I. Stream, Alexandra Galli, Veronica Pise-Masison, Cynthia A. Tagawa, Takanobu Ziegelbauer, Joseph M. Franchini, Genoveffa Yarchoan, Robert |
author_sort | Davis, David A. |
collection | PubMed |
description | Most chronic viruses evade T-cell and natural killer (NK) immunity through downregulation of immune surface markers. Previously we showed that Pomalidomide (Pom) increases surface expression of major histocompatibility complex class I (MHC-I) in Kaposi sarcoma-associated herpesvirus-infected latent and lytic cells and restores ICAM-1 and B7-2 in latent cells. We explored the ability of Pom to increase immune surface marker expression in cells infected by other chronic viruses, including human T-cell leukemia virus type-1 (HTLV-1), Epstein-Barr virus (EBV), human papilloma virus (HPV), Merkel cell polyoma virus (MCV), and human immunodeficiency virus type-1 (HIV-1). Pom increased MHC-1, ICAM-1, and B7-2/CD86 in immortalized T-cell lines productively infected with HTLV-1 and also significantly increased their susceptibility to NK cell-mediated cytotoxicity. Pom enhancement of MHC-I and ICAM-1 in primary cells infected with HTLV-1 was abrogated by knockout of HTLV-1 orf-1. Pom increased expression of ICAM-1, B7-2 and MHC class I polypeptide related sequence A (MICA) surface expression in the EBV-infected Daudi cells and increased their T-cell activation and susceptibility to NK cells. Moreover, Pom increased expression of certain of these surface markers on Akata, Raji, and EBV lymphoblastic cell lines. The increased expression of immune surface markers in these virus-infected lines was generally associated with a decrease in IRF4 expression. By contrast, Pom treatment of HPV, MCV and HIV-1 infected cells did not increase these immune surface markers. Pom and related drugs may be clinically beneficial for the treatment of HTLV-1 and EBV-induced tumors by rendering infected cells more susceptible to both innate and adaptive host immune responses. |
format | Online Article Text |
id | pubmed-6343774 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-63437742019-02-01 Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells Davis, David A. Shrestha, Prabha Aisabor, Ashley I. Stream, Alexandra Galli, Veronica Pise-Masison, Cynthia A. Tagawa, Takanobu Ziegelbauer, Joseph M. Franchini, Genoveffa Yarchoan, Robert Oncoimmunology Original Research Most chronic viruses evade T-cell and natural killer (NK) immunity through downregulation of immune surface markers. Previously we showed that Pomalidomide (Pom) increases surface expression of major histocompatibility complex class I (MHC-I) in Kaposi sarcoma-associated herpesvirus-infected latent and lytic cells and restores ICAM-1 and B7-2 in latent cells. We explored the ability of Pom to increase immune surface marker expression in cells infected by other chronic viruses, including human T-cell leukemia virus type-1 (HTLV-1), Epstein-Barr virus (EBV), human papilloma virus (HPV), Merkel cell polyoma virus (MCV), and human immunodeficiency virus type-1 (HIV-1). Pom increased MHC-1, ICAM-1, and B7-2/CD86 in immortalized T-cell lines productively infected with HTLV-1 and also significantly increased their susceptibility to NK cell-mediated cytotoxicity. Pom enhancement of MHC-I and ICAM-1 in primary cells infected with HTLV-1 was abrogated by knockout of HTLV-1 orf-1. Pom increased expression of ICAM-1, B7-2 and MHC class I polypeptide related sequence A (MICA) surface expression in the EBV-infected Daudi cells and increased their T-cell activation and susceptibility to NK cells. Moreover, Pom increased expression of certain of these surface markers on Akata, Raji, and EBV lymphoblastic cell lines. The increased expression of immune surface markers in these virus-infected lines was generally associated with a decrease in IRF4 expression. By contrast, Pom treatment of HPV, MCV and HIV-1 infected cells did not increase these immune surface markers. Pom and related drugs may be clinically beneficial for the treatment of HTLV-1 and EBV-induced tumors by rendering infected cells more susceptible to both innate and adaptive host immune responses. Taylor & Francis 2018-12-05 /pmc/articles/PMC6343774/ /pubmed/30713808 http://dx.doi.org/10.1080/2162402X.2018.1546544 Text en This work was authored as part of the Contributor’s official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article that has been identified as being free of known restrictions under copyright law, including all related and neighboring rights (https://creativecommons.org/publicdomain/mark/1.0/). You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission. |
spellingShingle | Original Research Davis, David A. Shrestha, Prabha Aisabor, Ashley I. Stream, Alexandra Galli, Veronica Pise-Masison, Cynthia A. Tagawa, Takanobu Ziegelbauer, Joseph M. Franchini, Genoveffa Yarchoan, Robert Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title | Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title_full | Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title_fullStr | Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title_full_unstemmed | Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title_short | Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
title_sort | pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343774/ https://www.ncbi.nlm.nih.gov/pubmed/30713808 http://dx.doi.org/10.1080/2162402X.2018.1546544 |
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