Linked Life Data

15553709

Source:http://linkedlifedata.com/resource/pubmed/id/15553709

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2004-11-19
pubmed:abstractText
Although we have reported that Toll-like receptor (TLR) 4 is involved in OK-432-induced anti-cancer immunity, its detailed mechanism remained uncertain. We hypothesized that OK-432 may first be captured, dissolved by phagocytes, and then active components released from the cells may stimulate TLR4. This hypothesis was examined by the current in vitro experiments. We used TS-2 MoAb which recognizes OK-PSA, an active component of OK-432. First, we observed that OK-432-induced cytokine production by dendritic cells (DCs) and macrophages was significantly inhibited by cytochalasin B, a phagocytosis inhibitor. Immunofluorescence staining by using TS-2 clearly demonstrated that OK-432 was captured and dissolved by these cells. OK-PSA was detected in the supernatants derived from OK-432-treated DC culture by ELISA with TS-2. The supernatants from OK-432-treated DC culture, but not from untreated DC culture, increased NF-kappaB activity in TLR4-expressing cells. The increased NF-kappaB activity was inhibited by TS-2. These findings elucidated the mechanism mediated by phagocytosis and TLR4 signaling in the OK-432 action.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0385-0684
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1767-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
[Analysis of the immuno-activation mechanism of OK-432--phagocytosis, release of active components and TLR4 signaling].
pubmed:affiliation
Second Dept. of Oral and Maxillofacial Surgery, Tokushima University School of Dentistry.
pubmed:publicationType
Journal Article, In Vitro, English Abstract