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Immune evasion is a strategy used by pathogenic organisms and tumours to evade a host's immune response to maximize their probability of being transmitted to a fresh host or to continue growing, respectively.
Cells infected with Epstein-Barr virus (EBV) express the virus-encoded EBNA1, which is essential for viral genome maintenance but also highly antigenic. Here the authors implicate nucleolin as a host factor that mediates the repression of EBNA1-derived antigenic peptides through binding of the G4-quadruplex structure present within the EBNA1 mRNA.
This Review examines accumulating evidence that translation arrest and stress granule formation can have antiviral properties through several mechanisms that are not limited to direct effects on the translation of viral proteins.
CD226 is an activating receptor expressed in a co-varied manner with inhibitory receptors on natural killer (NK) cells, but whether CD226 is involved in NK cell education is unclear. Here the authors show that CD226 expression is plastic depending on the MHC environment and endows educated NK cells enhanced effector functions.
A recent article published in Nature describes a novel genetic mechanism of immune evasion in a number of cancers that is caused by structural variants (SVs) disrupting the 3′ regulatory region of programmed cell death ligand 1 (PDL1).