Journal
IMMUNITY
Volume 13, Issue 3, Pages 365-374Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(00)00036-4
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Funding
- NATIONAL CANCER INSTITUTE [R01CA082057, R01CA031363, R01CA086841] Funding Source: NIH RePORTER
- NCI NIH HHS [CA86841, CA31363, CA82057] Funding Source: Medline
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Kaposi's sarcoma-associated herpesvirus (KSHV) K3 and K5 proteins dramatically downregulate MHC class I molecules. However, although MHC class I downregulation may protect KSHV-infected cells from cytotoxic T lymphocyte recognition, these cells become potential targets for natural killer (NK) cell-mediated lysis. We now show that K5 also downregulates ICAM-1 and B7-2, which are ligands for NK cell-mediated cytotoxicity receptors. As a consequence, K5 expression drastically inhibits NK cell-mediated cytotoxicity. Conversely, de novo expression of B7-2 and ICAM-1 resensitizes the W-expressing cells to NK cell-mediated cytotoxicity. This is a novel viral immune evasion strategy where KSHV K5 achieves immune avoidance by downregulation of cellular ligands for NK cell-mediated cytotoxicity receptors.
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