Granzyme K-deficient mice show no evidence of impaired antiviral immunity.

Immunol Cell Biol

Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

Published: September 2017

AI Article Synopsis

  • Granzyme K, a serine protease from cytotoxic T lymphocytes, is debated for its role in inducing cell death versus involvement in inflammation.
  • Gene deletion studies in mice (Gzmk) show that they are healthy and recover normally from viral infections, indicating no critical role for granzyme K in immunity.
  • The study concludes that granzyme K does not significantly impact viral immunity or cytotoxic functions, helping to fill gaps in understanding its biological roles.

Article Abstract

The biological role of granzyme K, a serine protease of cytotoxic T lymphocytes (CTL), is controversial. It has been reported to induce perforin-mediated cell death in vitro, but is also reported to be non-cytotoxic and to operate in inflammatory processes. To elucidate the biological role of this protease, we have deleted the granzyme K gene in mice (mutant allele: Gzmk; MGI:5636646). Gzmk mice are healthy, anatomically normal, fecund and show normal hematopoietic development. Gzmk mice readily recover from lymphocytic choriomeningitis virus and mouse pox Ectromelia virus infection. Ex vivo, virus-specific granzyme K-deficient CTL are indistinguishable from those of wild-type mice in apoptosis induction of target cells. These data suggest that granzyme K does not play an essential role in viral immunity or cytotoxicity. Our granzyme K knockout line completes the collection of mouse models for the human granzymes, and will further our understanding of their biological roles and relationships.

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Source
http://dx.doi.org/10.1038/icb.2017.35DOI Listing

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