Pomalidomide increases immune surface marker expression and immune recognition of oncovirus-infected cells.
CD86
ICAM-1
Natural killer (NK) cells
T cells
epstein barr virus (EBV)
human T lymphotropic virus type 1 (HTLV-1)
ikaros (IKZF1).
interferon regulatory factor 4 (IRF4)
major histocompatibility complex class I (MHC-I)
pomalidomide
Journal
Oncoimmunology
ISSN: 2162-4011
Titre abrégé: Oncoimmunology
Pays: United States
ID NLM: 101570526
Informations de publication
Date de publication:
Historique:
received:
15
06
2018
revised:
17
10
2018
accepted:
04
11
2018
entrez:
5
2
2019
pubmed:
5
2
2019
medline:
5
2
2019
Statut:
epublish
Résumé
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
Identifiants
pubmed: 30713808
doi: 10.1080/2162402X.2018.1546544
pii: 1546544
pmc: PMC6343774
doi:
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
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