| First Author | Joeckel LT | Year | 2017 |
| Journal | Immunol Cell Biol | Volume | 95 |
| Issue | 8 | Pages | 676-683 |
| PubMed ID | 28428612 | Mgi Jnum | J:302067 |
| Mgi Id | MGI:6507649 | Doi | 10.1038/icb.2017.35 |
| Citation | Joeckel LT, et al. (2017) Granzyme K-deficient mice show no evidence of impaired antiviral immunity. Immunol Cell Biol 95(8):676-683 |
| abstractText | 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. |
