Cytomegalovirus Infection Drives Avidity Selection of Natural Killer Cells.

Immunity

Immunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Louis V. Gerstner, Jr. Graduate School of Biomedical Sciences, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Department of Immunology and Microbial Pathogenesis, Weill Cornell Medical College, New York, NY 10065, USA. Electronic address:

Published: June 2019

AI Article Synopsis

  • * Researchers found that NK cells with the highest affinity for the CMV glycoprotein m157 were preferentially expanded in the memory NK cell pool, while those with lower affinity were better at producing interferon-γ (IFN-γ).
  • * The findings indicate that varying levels of NK cell avidity enhance their effectiveness during antiviral responses and suggest that affinity selection plays a role in developing potent memory NK cells in both mice and humans.

Article Abstract

The process of affinity maturation, whereby T and B cells bearing antigen receptors with optimal affinity to the relevant antigen undergo preferential expansion, is a key feature of adaptive immunity. Natural killer (NK) cells are innate lymphocytes capable of "adaptive" responses after cytomegalovirus (CMV) infection. However, whether NK cells are similarly selected on the basis of their avidity for cognate ligand is unknown. Here, we showed that NK cells with the highest avidity for the mouse CMV glycoprotein m157 were preferentially selected to expand and comprise the memory NK cell pool, whereas low-avidity NK cells possessed greater capacity for interferon-γ (IFN-γ) production. Moreover, we provide evidence for avidity selection occurring in human NK cells during human CMV infection. These results delineate how heterogeneity in NK cell avidity diversifies NK cell effector function during antiviral immunity, and how avidity selection might serve to produce the most potent memory NK cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614060PMC
http://dx.doi.org/10.1016/j.immuni.2019.04.009DOI Listing

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