4.3 Article

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

Journal

IMMUNOLOGY AND CELL BIOLOGY
Volume 95, Issue 8, Pages 676-683

Publisher

WILEY
DOI: 10.1038/icb.2017.35

Keywords

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Funding

  1. National Health and Medical Research Council (Australia) [490900, 1006592, 1045549, 1065626]
  2. Sylvia & Charles Viertel Senior Medical Fellowship
  3. German Research Council (Deutsche Forschungsgemeinschaft, DFG) [JO 1104/1-1]

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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(tm1.1Pib); 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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