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dc.contributor.authorKared, H
dc.contributor.authorMartelli, S
dc.contributor.authorTan, SW
dc.contributor.authorSimoni, Y
dc.contributor.authorChong, ML
dc.contributor.authorYap, SH
dc.contributor.authorNewell, EW
dc.contributor.authorPender, SLF
dc.contributor.authorKamaruizaman, A
dc.contributor.authorRajasuriar, R
dc.contributor.authorLarbi, A
dc.date.accessioned2020-12-10T01:32:51Z
dc.date.available2020-12-10T01:32:51Z
dc.date.issued2018-04-20
dc.identifier.citationKared, H., Martelli, S., Tan, S. W., Simoni, Y., Chong, M. L., Yap, S. H., Newell, E. W., Pender, S. L. F., Kamaruizaman, A., Rajasuriar, R. & Larbi, A. (2018). Adaptive NKG2C(+)CD57(+) Natural Killer Cell and Tim-3 Expression During Viral Infections. FRONTIERS IN IMMUNOLOGY, 9 (APR), https://doi.org/10.3389/fimmu.2018.00686.
dc.identifier.issn1664-3224
dc.identifier.urihttp://hdl.handle.net/11343/253731
dc.description.abstractRepetitive 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.
dc.languageEnglish
dc.publisherFRONTIERS MEDIA SA
dc.titleAdaptive NKG2C(+)CD57(+) Natural Killer Cell and Tim-3 Expression During Viral Infections
dc.typeJournal Article
dc.identifier.doi10.3389/fimmu.2018.00686
melbourne.affiliation.departmentDoherty Institute
melbourne.source.titleFrontiers in Immunology
melbourne.source.volume9
melbourne.source.issueAPR
dc.rights.licenseCC BY
melbourne.elementsid1326482
melbourne.contributor.authorRajasuriar, Reena
dc.identifier.eissn1664-3224
melbourne.accessrightsOpen Access


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