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Natural killer (NK) cells are equipped with anti-Epstein-Barr virus (EBV) function, however, whether EBV infection will affect NK cells reconstitution after allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains unclear. To identify the characteristics of NK cells, we prospectively enrolled 11 patients who occurred EBV reactivation post allo-HSCT and 11 patients without EBV infection as control. We found that that EBV infection induced the expansion of CD56bright and NKG2A+KIR− NK subsets,and decreased the cytotoxicity function of NK cells. The frequency of NKG2A+KIR- NK cells were higher in patients who progressed into post-transplant lymphoproliferative disorder (PTLD) than EBV viremia patients, which also correlated with decreased proliferation and cytotoxic function. By screening the activation receptors of NK cells, we found the DNAM-1+CD56bright NK cells is significantly increased after EBV stimulation, further we demonstrated that DNAM-1 is essential for EBV induced NK cells activation as the cytokine release against EBV-transformed lymphoblastoid cell lines(EBV-LCLs) of CD56bright NK cells were significantly decreased after DNAM-1 blockade. NK cells infusion suppressed the progression of EBV-related tumor mice model. A prospective cohort indicated that old donor age was an independent risk factor for EBV infection. Rapid CD56bri expansion and high expression of DNAM-1 on CD56bri NK cells in response to EBV reactivation correlated with rapid EBV clearance post allo-HSCT in patients with younger donors. In summary, our data showed that high expression of DNAM-1 receptors on NK cell may participate protective CD56bri NK cells response to EBV infection after allo-HSCT. [ABSTRACT FROM AUTHOR]

Reversible alternation between bipolar and unipolar resistive switching (RS) modes was observed by controlling voltage-polarity in Ag/MoS2/Au memory on polyethylene terephthalate (PET) substrate. The temperature-dependent low-resistance-state and Raman measurement indicated that Ag and sulphur vacancy (Vs)-based conductive filaments (CFs) were responsible for these two RS modes. The two kinds of CFs had different responses under positive read voltages. Thus, a new operation scheme of multilevel memory was demonstrated in which multiple states were distinguished by CF composition rather than resistance values. The memory capacity of the cell could be further extended by adjustments in CFs’ size in each mode. The RS performance of the device did not degrade under bending conditions even over 104 bending cycles, which indicated good mechanical flexibility. The present Ag/MoS2/Au memory has promise for future high-density flexible information storage. [ABSTRACT FROM AUTHOR]

Natural killer (NK) cells are lymphocytes that are involved in controlling tumors or microbial infections through the production of interferon gamma (IFN-γ). Granulocyte colony-stimulating factor (G-CSF) inhibits IFN-γ secretion by NK cells, but the mechanism underlying this effect remains unclear. Here, by comparing the multi-omics profiles of human NK cells before and after in vivo G-CSF treatment, we identify a pathway that is activated in response to G-CSF treatment, which suppresses IFN-γ secretion in NK cells. Specifically, glucocorticoid receptors (GRs) activated by G-CSF inhibit secretion of IFN-γ by promoting interactions between SOCS1 promoters and enhancers, as well as increasing the expression of SOCS1. Experiments in mice confirm that G-CSF treatment significantly downregulates IFN-γ secretion and upregulates GR and SOCS1 expression in NK cells. In addition, GR blockade by the antagonist RU486 significantly reverses the effects of G-CSF, demonstrating that GRs upregulate SOCS1 and inhibit the production of IFN-γ by NK cells. [Display omitted] • GRs are activated by G-CSF and mediate the genomic changes in NK cells • GR-SOCS1 axis suppresses IFN-γ secretion by NK cells • GRs promote chromatin interaction between SOCS1 promoter and enhancer • GR blocking reverses the effect of G-CSF on NK cells Zhao et al. reveal that GRs are the crucial factor that mediate the genomic and transcriptomic changes in NK cells after in vivo G-CSF mobilization. Activated GRs promote interactions between SOCS1 promoters and enhancers and increase the expression of SOCS1 , whose protein product inhibits the secretion of IFN-γ by NK cells. [ABSTRACT FROM AUTHOR]