2014
DOI: 10.1182/blood-2014-01-553024
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Role for early-differentiated natural killer cells in infectious mononucleosis

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Cited by 164 publications
(260 citation statements)
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References 58 publications
(55 reference statements)
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“…To date, apart from HCMV, no other viruses have been seen to correlate with the appearance of adaptive NK cells, and associated KIR repertoire deviations, including herpes simplex virus (both HSV‐1 and HSV‐2) and varicella‐zoster virus 160, 169. Instead, it was shown that acute Epstein–Barr virus infection induces NKG2A +  CD57 + expansion lacking KIR expression 170. Altogether, these findings suggest that KIR, and adaptive NK cells, might have mainly evolved to control HCMV.…”
Section: Kir Gene Expressionmentioning
confidence: 99%
“…To date, apart from HCMV, no other viruses have been seen to correlate with the appearance of adaptive NK cells, and associated KIR repertoire deviations, including herpes simplex virus (both HSV‐1 and HSV‐2) and varicella‐zoster virus 160, 169. Instead, it was shown that acute Epstein–Barr virus infection induces NKG2A +  CD57 + expansion lacking KIR expression 170. Altogether, these findings suggest that KIR, and adaptive NK cells, might have mainly evolved to control HCMV.…”
Section: Kir Gene Expressionmentioning
confidence: 99%
“…1,2 Recently, Azzi et al described the role of early differentiated NK cells in Epstein-Barr virus-driven infectious mononucleosis (IM). 3 Besides the conventional CD56 bright CD16 Figure 1A). Blood samples were obtained from 9 pediatric HSCT recipients and 4 healthy donors with written informed consent and approval by the Institutional Review Board (protocol P02.099).…”
mentioning
confidence: 99%
“…Interestingly, and in contrast to the prototypic terminally differentiated NK cell-expanding pathogen HCMV, EBV seems to drive the proliferation of early differentiated non-KIR-educated NK cells (25,27). These NK cells have been reported to recognize B cells that lytically replicate EBV via recognition by the activating NK cell receptors NKG2D and DNAM-1 (28), and the respective ligands for these receptors seem to be upregulated during transition from latent to lytic EBV infection (25,28). Loss of NK cells leads to elevated viral loads of WT, but not lytic replication-incompetent, EBV in vivo (26).…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, donors were disparate for HLA-A2 expression, which allowed us to track the progeny of specific donors in mixed reconstitution lial malignancies through its viral oncogenes that are expressed during latent infection, lytic replication that produces infectious virions seems to be poorly controlled during IM and causes the characteristic immune pathogenic CD8 + T cell lymphocytosis of this disease (23). NK cells were reported to expand during IM (21,24,25) and seem to particularly restrict lytic EBV infection that is deregulated during IM (25,26). Interestingly, and in contrast to the prototypic terminally differentiated NK cell-expanding pathogen HCMV, EBV seems to drive the proliferation of early differentiated non-KIR-educated NK cells (25,27).…”
Section: Resultsmentioning
confidence: 99%
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