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  Human and Mouse Granzyme A Induce a Proinflammatory Cytokine Response

Metkar, S. S., Menaa, C., Pardo, J., Wang, B., Wallich, R., Freudenberg, M., et al. (2008). Human and Mouse Granzyme A Induce a Proinflammatory Cytokine Response. Immunity, 29, 720-733.

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 Creators:
Metkar, Sunil S., Author
Menaa, Cheikh, Author
Pardo, Julian1, Author              
Wang, Baikun, Author
Wallich, Reinhard, Author
Freudenberg, Marina2, Author              
Kim, Stephen, Author
Raja, Srikumar, Author
Shi, Lianfa, Author
Simon, Markus M.1, Author              
Froelich, Christopher J., Author
Affiliations:
1Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243654              
2Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              

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 Abstract: Granzyme A (GzmA) is considered a major proapoptotic protease. We have discovered that GzmA-induced cell death involves rapid membrane damage that depends on the synergy between micromolar concentrations of GzmA and sublytic perforin (PFN). Ironically, GzmA and GzmB, independent of their catalytic activity, both mediated this swift necrosis. Even without PFN, lower concentrations of human GzmA stimulated monocytic cells to secrete proinflammatory cytokines (interleukin-1β [IL-1β], TNFα, and IL-6) that were blocked by a caspase-1 inhibitor. Moreover, murine GzmA and GzmA+ cytotoxic T lymphocytes (CTLs) induce IL-1β from primary mouse macrophages, and GzmA-/- mice resist lipopolysaccharide-induced toxicity. Thus, the granule secretory pathway plays an unexpected role in inflammation, with GzmA acting as an endogenous modulator.

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Language(s): eng - English
 Dates: 2008-11-14
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 400830
 Degree: -

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Title: Immunity
Source Genre: Journal
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Pages: - Volume / Issue: 29 Sequence Number: - Start / End Page: 720 - 733 Identifier: -