Journal
CELL REPORTS
Volume 35, Issue 5, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2021.109056
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Funding
- Cancer Research Switzerland, Switzerland [KFS-4091-02-2017]
- KFSP-PrecisionMS and HMZ ImmunoTargET of the University of Zurich, Switzerland
- Cancer Research Center Zurich, Switzerland
- Vontobel Foundation, Switzerland
- Baugarten Foundation, Switzerland
- Sobek Foundation, Germany
- Swiss Vaccine Research Institute, Switzerland
- Roche, Switzerland
- Novartis, Switzerland
- Swiss National Science Foundation, Switzerland [310030B_182827, CRSII5_180323]
- National Institutes of Health, United States [R01 CA189806]
- career advancement grant from the University of Zurich, Switzerland [FK-18-026]
- Swiss National Science Foundation, Switzerland
- Swiss Academy of Medical Sciences, Switzerland [323530_145247, 323630_19938]
- Swiss National Science Foundation (SNF) [323530_145247] Funding Source: Swiss National Science Foundation (SNF)
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Herpesvirus infections, such as EBV, CMV, and KSHV, impact the composition of human NK cells, leading to the accumulation of specific NK cell subsets. KSHV infection may evade NK cell-mediated immune control through driving the differentiation of a specific NK cell subset, CD56(-)CD16(+) NK cells.
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.
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