
doi: 10.1038/icb.2017.35
pmid: 28428612
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: Gzmktm1.1Pib; 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.
Cytotoxicity, Immunologic, Mice, Knockout, Ectromelia virus, Lymphocytic Choriomeningitis, Lymphocyte Activation, Granzymes, Hematopoiesis, Mice, Inbred C57BL, Mice, Animals, Lymphocytic choriomeningitis virus, Ectromelia, Infectious, Antigens, Viral, Cells, Cultured, T-Lymphocytes, Cytotoxic
Cytotoxicity, Immunologic, Mice, Knockout, Ectromelia virus, Lymphocytic Choriomeningitis, Lymphocyte Activation, Granzymes, Hematopoiesis, Mice, Inbred C57BL, Mice, Animals, Lymphocytic choriomeningitis virus, Ectromelia, Infectious, Antigens, Viral, Cells, Cultured, T-Lymphocytes, Cytotoxic
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