rdf:type |
|
lifeskim:mentions |
umls-concept:C0003864,
umls-concept:C0017262,
umls-concept:C0021368,
umls-concept:C0087111,
umls-concept:C0443146,
umls-concept:C0597357,
umls-concept:C0887899,
umls-concept:C1171362,
umls-concept:C1515670,
umls-concept:C1706099,
umls-concept:C1948041
|
pubmed:issue |
6
|
pubmed:dateCreated |
2009-6-16
|
pubmed:abstractText |
Triggering receptor expressed on myeloid cells 1 (TREM-1) is inducible on monocyte/macrophages and neutrophils and accelerates tissue destruction by propagating inflammatory responses in disease related to bacterial infections. Its blockade rescues the hosts in murine models of sepsis, to clear the bacteria without impairing the host defense. The aim of this study was to investigate the involvement of TREM-1 in an autoimmune, noninfectious disease.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
0004-3591
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
60
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1615-23
|
pubmed:meshHeading |
pubmed-meshheading:19479878-Animals,
pubmed-meshheading:19479878-Arthritis, Experimental,
pubmed-meshheading:19479878-Arthritis, Rheumatoid,
pubmed-meshheading:19479878-Autoimmune Diseases,
pubmed-meshheading:19479878-Cells, Cultured,
pubmed-meshheading:19479878-Dinoprostone,
pubmed-meshheading:19479878-Disease Models, Animal,
pubmed-meshheading:19479878-Humans,
pubmed-meshheading:19479878-Immunoglobulin G,
pubmed-meshheading:19479878-Inflammation Mediators,
pubmed-meshheading:19479878-Macrophages,
pubmed-meshheading:19479878-Male,
pubmed-meshheading:19479878-Membrane Glycoproteins,
pubmed-meshheading:19479878-Mice,
pubmed-meshheading:19479878-Mice, Inbred DBA,
pubmed-meshheading:19479878-Peptides,
pubmed-meshheading:19479878-Receptors, Immunologic,
pubmed-meshheading:19479878-Synovial Membrane,
pubmed-meshheading:19479878-Up-Regulation
|
pubmed:year |
2009
|
pubmed:articleTitle |
Intervention of an inflammation amplifier, triggering receptor expressed on myeloid cells 1, for treatment of autoimmune arthritis.
|
pubmed:affiliation |
Tokyo Medical and Dental University, Department of Medicine and Rheumatology, Graduate School, Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|