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Calcium mobilizing treatment acts as a co-signal for TLR-mediated induction of Interleukin-12 (IL-12p70) secretion by murine bone marrow-derived dendritic cells
被引:7
|作者:
Huang, Emily
[1
]
Showalter, Loral
[1
]
Xu, Shuwen
[1
]
Czernliecki, Brian J.
[1
]
Koski, Gary K.
[1
]
机构:
[1] Kent State Univ, Dept Biol Sci, Sch Biomed Sci, Kent, OH 44242 USA
关键词:
Dentritic cell;
IL-12;
Toll-like receptor;
Calcium mobilization;
Th polarization;
D O I:
10.1016/j.cellimm.2017.01.010
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
We sought to determine whether pharmacological calcium-mobilizing agents could act in cooperation with Toll-like receptor (TLR) signals to induce high-level IL-12 production from murine bone marrow derived dendritic cells. We found that calcium mobilization alone induced no IL-12, yet dramatically enhanced IL-12p70 secretion elicited by TLR ligands. Enhanced IL-12 production induced by calcium ionophore plus single TLR ligands, but not through dual TLR ligands, was inhibited by the calcineurin antagonist cyclosporine A, suggesting divergent mechanisms of IL-12 induction. Dendritic cells activated with calciumionophore plus the TLR9 ligand ODN1826 could induce Th1 polarization in nave murine CD4(POS) T cells at levels equal or superior to dendritic cells activated with the most efficient TLR ligand pairing; ODN1826 plus bacterial lipopolysaccharide. Parallel analysis of 38 inflammation-associated soluble products showed calciumionophore enhancement was restricted to a small set of factors. These data demonstrate previously undocumented activation co-signals for IL-12 production by dendritic cells. (C) 2017 Elsevier Inc. All rights reserved.
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页码:26 / 35
页数:10
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