Please use this identifier to cite or link to this item:
https://doi.org/10.3389/fimmu.2018.00686
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 apoptosis Article enzyme linked immunosorbent assay flow cytometry human Human immunodeficiency virus infection immune response matrix assisted laser desorption ionization time of flight mass spectrometry natural killer cell phenotype 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. https://doi.org/10.3389/fimmu.2018.00686 | 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 | URI: | https://scholarbank.nus.edu.sg/handle/10635/174540 | ISSN: | 16643224 | DOI: | 10.3389/fimmu.2018.00686 |
Appears in Collections: | Elements Staff Publications |
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