NK cell intrinsic regulation of MIP-1α by granzyme M

Baschuk, N., Wang, N., Watt, S. V., Halse, H., House, C., Bird, P. I., Strugnell, R., Trapani, J. A., Smyth, M. J. and Andrews, D. M. (2014) NK cell intrinsic regulation of MIP-1α by granzyme M. Cell Death and Disease, 5 . doi:10.1038/cddis.2014.74


Author Baschuk, N.
Wang, N.
Watt, S. V.
Halse, H.
House, C.
Bird, P. I.
Strugnell, R.
Trapani, J. A.
Smyth, M. J.
Andrews, D. M.
Title NK cell intrinsic regulation of MIP-1α by granzyme M
Formatted title
NK cell intrinsic regulation of MIP-1α by granzyme M
Journal name Cell Death and Disease   Check publisher's open access policy
ISSN 2041-4889
Publication date 2014-03-13
Sub-type Article (original research)
DOI 10.1038/cddis.2014.74
Open Access Status DOI
Volume 5
Total pages 11
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Collection year 2015
Language eng
Formatted abstract
Granzymes are generally recognized for their capacity to induce various pathways of perforin-dependent target cell death. Within this serine protease family, Granzyme M (GrzM) is unique owing to its preferential expression in innate effectors such as natural killer (NK) cells. During Listeria monocytogenes infection, we observed markedly reduced secretion of macrophage inflammatory protein-1 alpha (MIP-1α) in livers of GrzM-deficient mice, which resulted in significantly impaired NK cell recruitment. Direct stimulation with IL-12 and IL-15 demonstrated that GrzM was required for maximal secretion of active MIP-1α. This effect was not due to reduced protein induction but resulted from heightened intracellular accumulation of MIP-1α, with reduced release. These results demonstrate that GrzM is a critical mediator of innate immunity that can regulate chemotactic networks and has an important role in the initiation of immune responses and pathogen control.
Keyword NK cells
Granzyme M
MIP-1α
Listeria monocytogenes infection
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Article ID: e1115

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Medicine Publications
 
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