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Title: Adaptive NKG2C+CD57+ natural killer cell and Tim-3 expression during viral infections
Authors: Kared, H.
Martelli, S.
Tan, S.W.
Simoni, Y.
Chong, M.L.
Yap, S.H.
Newell, E.W.
Pender, S.L.F.
Kamarulzaman, A.
Rajasuriar, R.
Larbi, A. 
Keywords: activated prothrombin complex
gamma interferon
zinc finger protein
enzyme linked immunosorbent assay
flow cytometry
Human immunodeficiency virus infection
immune response
matrix assisted laser desorption ionization time of flight mass spectrometry
natural killer cell
real time polymerase chain reaction
RNA interference
virus infection
Issue Date: 2018
Publisher: Frontiers Media S.A.
Citation: Kared, H., Martelli, S., Tan, S.W., Simoni, Y., Chong, M.L., Yap, S.H., Newell, E.W., Pender, S.L.F., Kamarulzaman, A., Rajasuriar, R., Larbi, A. (2018). Adaptive NKG2C+CD57+ natural killer cell and Tim-3 expression during viral infections. Frontiers in Immunology 9 (APR) : 686. ScholarBank@NUS Repository.
Abstract: Repetitive stimulation by persistent pathogens such as human cytomegalovirus (HCMV) or human immunodeficiency virus (HIV) induces the differentiation of natural killer (NK) cells. This maturation pathway is characterized by the acquisition of phenotypic markers, CD2, CD57, and NKG2C, and effector functions-a process regulated by Tim-3 and orchestrated by a complex network of transcriptional factors, involving T-bet, Eomes, Zeb2, promyelocytic leukemia zinc finger protein, and Foxo3. Here, we show that persistent immune activation during chronic viral co-infections (HCMV, hepatitis C virus, and HIV) interferes with the functional phenotype of NK cells by modulating the Tim-3 pathway; a decrease in Tim-3 expression combined with the acquisition of inhibitory receptors skewed NK cells toward an exhausted and cytotoxic phenotype in an inflammatory environment during chronic HIV infection. A better understanding of the mechanisms underlying NK cell differentiation could aid the identification of new immunological targets for checkpoint blockade therapies in a manner that is relevant to chronic infection and cancer. © 2018 Kared, Martelli, Tan, Simoni, Chong, Yap, Newell, Pender, Kamarulzaman, Rajasuriar and Larbi.
Source Title: Frontiers in Immunology
ISSN: 16643224
DOI: 10.3389/fimmu.2018.00686
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