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Journal Article

Mouse granzyme K has pro-inflammatory potential

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Joeckel,  L. T.
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Martin,  P.
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Pardo,  J.
Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Simon,  M. M.
Max Planck Society;

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Citation

Joeckel, L. T., Wallich, R., Martin, P., Sanchez-Martinez, D., Weber, F. C., Martin, S. F., et al. (2011). Mouse granzyme K has pro-inflammatory potential. Cell Death and Differentiation, 18, 1112-1119.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-8E0D-B
Abstract
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-1β, independent of the ATP receptor P2X7. 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.