Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1 - 11 |
| Number of pages | 11 |
| Journal | Cell Death and Disease |
| Volume | 5 |
| Issue number | 3 (Art. No.: e1115) |
| DOIs | |
| Publication status | Published - 2014 |
Cite this
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NK cell intrinsic regulation of MIP-1alpha by granzyme M. / Baschuk, Nikola; Wang, Nancy; Watt, Sally V; Halse, Heloise M; House, Colin M; Bird, Phillip Ian; Strugnell, Richard Anthony; Trapani, Joseph A; Smyth, Mark; Andrews, Daniel M.
In: Cell Death and Disease, Vol. 5, No. 3 (Art. No.: e1115), 2014, p. 1 - 11.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - NK cell intrinsic regulation of MIP-1alpha by granzyme M
AU - Baschuk, Nikola
AU - Wang, Nancy
AU - Watt, Sally V
AU - Halse, Heloise M
AU - House, Colin M
AU - Bird, Phillip Ian
AU - Strugnell, Richard Anthony
AU - Trapani, Joseph A
AU - Smyth, Mark
AU - Andrews, Daniel M
PY - 2014
Y1 - 2014
N2 - 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-1alpha) 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-1alpha. This effect was not due to reduced protein induction but resulted from heightened intracellular accumulation of MIP-1alpha, 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.
AB - 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-1alpha) 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-1alpha. This effect was not due to reduced protein induction but resulted from heightened intracellular accumulation of MIP-1alpha, 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.
UR - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973215/pdf/cddis201474a.pdf
U2 - 10.1038/cddis.2014.74
DO - 10.1038/cddis.2014.74
M3 - Article
VL - 5
SP - 1
EP - 11
JO - Cell Death and Disease
JF - Cell Death and Disease
SN - 2041-4889
IS - 3 (Art. No.: e1115)
ER -