Of tumor microenvironments or viral infection results in a reduced Dysregulation of theīalance between inhibitory and activating signaling in the context
Is tightly regulated by two classes of NK receptors, inhibitory receptorsĪnd activating NK receptors, which engage ligands, such as MHC I,Īnd in turn tune the level of NK cell activity. These results uncover a strategy for enhancing the activity of NKĪnd T cells that may improve cancer immunotherapies.Īgainst infection and cancer. Possible CD45 segregation within the NK cell-target cell synapse. Of weak inhibition from engagement of MHC I on non-target cells, and Other mechanisms, including avidity effects, tonic signaling, antagonism Signaling from engagement of MHC I on target cells, combined with The basis of the activityĮnhancement by CD45 ligation may reflect greater antagonism of inhibitory In their ability to enhance NK cell activation. That collectively inhibit NK cell activation, such that CD45–NKG2AĪnd CD45–Ly49 bispecific molecules show synergistic effects We also uncovered crosstalk between NKG2A and Ly49 To a VHH that binds the cell surface phosphatase CD45 potentiate NKĪnd T activities to a greater extent than NKR blocking antibodiesĪlone in vitro. Here, we find that single-chain NKR antagonists linked Play a key role in suppressing NK activity upon engagement with tumorĬells or virus-infected cells, limiting their antitumor and antiviralĪctivities. Two main classes of inhibitory NK receptors (NKR), KIR and CD94/NKG2A, That are essential for host defense against pathogens and cancer. Natural killer (NK) cells are a major subset of innate
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