| First Author | Joeckel LT | Year | 2011 |
| Journal | Cell Death Differ | Volume | 18 |
| Issue | 7 | Pages | 1112-9 |
| PubMed ID | 21311565 | Mgi Jnum | J:203106 |
| Mgi Id | MGI:5524219 | Doi | 10.1038/cdd.2011.5 |
| Citation | Joeckel LT, et al. (2011) Mouse granzyme K has pro-inflammatory potential. Cell Death Differ 18(7):1112-9 |
| abstractText | Granzymes (gzms) are key components of T-killer (Tc) cells believed to mediate pro-apoptotic activities. Recent evidence suggests that gzms also possess non-cytotoxic activities that contribute to host defense. In this study, we show that Tc cells from lymphocytic choriomeningitis virus (LCMV)-infected wild-type (wt) and gzm A/B-deficient mice express similar levels of gzmK protein, with both mouse strains efficiently controlling infection. GzmK, in recombinant form or secreted by ex vivo-derived LCMV-immune gzmAxB(-/-) Tc cells, lacks pro-apoptotic activity. Instead, gzmK induces primary mouse macrophages to process and secrete interleukin-1beta, independent of the ATP receptor P2X(7). Together with the finding that IL-1Ra (Anakinra) treatment inhibits virus elimination but not generation of cytotoxic Tc cells in wt mice, the data suggest that Tc cells control LCMV through non-cytotoxic processes that involve gzmK. |
