Reversal of TREM-1 ectodomain shedding and improved bacterial clearance by intranasal metalloproteinase inhibitors.

about

Reversal of TREM-1 ectodomain shedding and improved bacterial clearance by intranasal metalloproteinase inhibitors.

Item

http://www.wikidata.org/entity/Q40410587

description

2016 nî lūn-bûn

@nan

2016年の論文

@ja

2016年論文

@yue

2016年論文

@zh-hant

2016年論文

@zh-hk

2016年論文

@zh-mo

2016年論文

@zh-tw

2016年论文

@wuu

2016年论文

@zh

2016年论文

@zh-cn

name

Reversal of TREM-1 ectodomain ...... metalloproteinase inhibitors.

@en

type

Item

label

Reversal of TREM-1 ectodomain ...... metalloproteinase inhibitors.

@en

prefLabel

Reversal of TREM-1 ectodomain ...... metalloproteinase inhibitors.

@en

P1476

Reversal of TREM-1 ectodomain ...... metalloproteinase inhibitors.

@en

P2093

C Lai

http://www.w3.org/2001/XMLSchema#string

G Weiss

http://www.w3.org/2001/XMLSchema#string

G Xin

http://www.w3.org/2001/XMLSchema#string

M E Fife

http://www.w3.org/2001/XMLSchema#string

R J Snelgrove

http://www.w3.org/2001/XMLSchema#string

T Hussell

http://www.w3.org/2001/XMLSchema#string

P2860

TREM-1 amplifies inflammation and is a crucial mediator of septic shock

TREM-1, MDL-1, and DAP12 expression is associated with a mature stage of myeloid development

Transepithelial migration of neutrophils into the lung requires TREM-1

L-selectin: mechanisms and physiological significance of ectodomain cleavage.

Pulmonary matrix metalloproteinase-9 activity in mechanically ventilated children with respiratory syncytial virus.

Dynamic changes of serum soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) reflect sepsis severity and can predict prognosis: a prospective study.

Matrix metalloprotease 9 mediates neutrophil migration into the airways in response to influenza virus-induced toll-like receptor signaling.

MMP-9 cleaves SP-D and abrogates its innate immune functions in vitro

Modulation of the triggering receptor expressed on the myeloid cell type 1 pathway in murine septic shock

Lowering the threshold of lung innate immune cell activation alters susceptibility to secondary bacterial superinfection

P2888

mi.2016.104

P304

1021-1030

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1038/MI.2016.104

http://www.w3.org/2001/XMLSchema#string

P433

http://www.w3.org/2001/XMLSchema#string

P478

http://www.w3.org/2001/XMLSchema#string

P50

Aleksander M. Grabiec

Clare M. Lloyd

Bernadett Tildy

P577

2016-12-14T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P6179

1038168593

http://www.w3.org/2001/XMLSchema#string

P698

27966555

http://www.w3.org/2001/XMLSchema#string