KSHV infection drives poorly cytotoxic CD56-negative natural killer cell differentiation in vivo upon KSHV/EBV dual infection
| Autor: | Peter O Oluoch, Ann M. Moormann, Lara Zuppiger, Nicole Caduff, Thomas F. Schulz, David J. Blackbourn, Lisa Rieble, Christian Münz, Anita Murer, Ana Raykova, Obinna Chijioke, Donal McHugh, John M. Ong’echa, Catherine Forconi, Michelle Böni |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Human cytomegalovirus Epstein-Barr Virus Infections humanized mouse model QH301-705.5 viruses Cell chemical and pharmacologic phenomena KSHV Biology CD38 medicine.disease_cause Kaposi sarcoma-associated herpesvirus General Biochemistry Genetics and Molecular Biology Virus Natural killer cell differentiation Mice 03 medical and health sciences 0302 clinical medicine EBV hemic and lymphatic diseases medicine Animals Humans Cytotoxic T cell Epstein-Barr virus Biology (General) natural killer cells virus diseases Cell Differentiation biochemical phenomena metabolism and nutrition medicine.disease Virology Epstein–Barr virus Killer Cells Natural 030104 developmental biology medicine.anatomical_structure Herpesvirus 8 Human Primary effusion lymphoma 030217 neurology & neurosurgery |
| Zdroj: | Cell Reports, Vol 35, Iss 5, Pp 109056-(2021) |
| ISSN: | 2211-1247 |
| Popis: | Summary Herpesvirus infections shape the human natural killer (NK) cell compartment. While Epstein-Barr virus (EBV) expands immature NKG2A+ NK cells, human cytomegalovirus (CMV) drives accumulation of adaptive NKG2C+ NK cells. Kaposi sarcoma-associated herpesvirus (KSHV) is a close relative of EBV, and both are associated with lymphomas, including primary effusion lymphoma (PEL), which nearly always harbors both viruses. In this study, KSHV dual infection of mice with reconstituted human immune system components leads to the accumulation of CD56–CD16+CD38+CXCR6+ NK cells. CD56–CD16+ NK cells were also more frequently found in KSHV-seropositive Kenyan children. This NK cell subset is poorly cytotoxic against otherwise-NK-cell-susceptible and antibody-opsonized targets. Accordingly, NK cell depletion does not significantly alter KSHV infection in humanized mice. These data suggest that KSHV might escape NK-cell-mediated immune control by driving CD56–CD16+ NK cell differentiation. |
| Databáze: | OpenAIRE |
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