| pubmed-article:17540734 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17540734 | lifeskim:mentions | umls-concept:C1411976 | lld:lifeskim |
| pubmed-article:17540734 | lifeskim:mentions | umls-concept:C0041221 | lld:lifeskim |
| pubmed-article:17540734 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
| pubmed-article:17540734 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
| pubmed-article:17540734 | lifeskim:mentions | umls-concept:C0871161 | lld:lifeskim |
| pubmed-article:17540734 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17540734 | pubmed:dateCreated | 2007-8-28 | lld:pubmed |
| pubmed-article:17540734 | pubmed:abstractText | We have demonstrated recently that the glycoinositolphospholipid (GIPL) molecule from the protozoan Trypanosoma cruzi is a TLR4 agonist with proinflammatory effects. Here, we show that GIPL-induced neutrophil recruitment into the peritoneal cavity is mediated by at least two pathways: one, where IL-1beta acts downstream of TNF-alpha, and a second, which is IL-1beta- and TNFRI-independent. Moreover, NKT cells participate in this proinflammatory cascade, as in GIPL-treated CD1d(-/-) mice, TNF-alpha and MIP-2 levels are reduced significantly. As a consequence of this inflammatory response, spleen and lymph nodes of GIPL-treated mice have an increase in the percentage of T and B cells expressing the CD69 activation marker. Cell-transfer experiments demonstrate that T and B cell activation by GIPL is an indirect effect, which relies on the expression of TLR4 by other cell types. Moreover, although signaling through TNFRI contributes to the activation of B and gammadelta+ T cells, it is not required for increasing CD69 expression on alphabeta+ T lymphocytes. It is interesting that T cells are also functionally affected by GIPL treatment, as spleen cells from GIPL-injected mice show enhanced production of IL-4 following in vitro stimulation by anti-CD3. Together, these results contribute to the understanding of the inflammatory properties of the GIPL molecule, pointing to its potential role as a parasite-derived modulator of the immune response during T. cruzi infection. | lld:pubmed |
| pubmed-article:17540734 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17540734 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17540734 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17540734 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17540734 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:17540734 | pubmed:issn | 0741-5400 | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:Van KaerLucL | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:PreviatoJosé... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:Mendonça-Prev... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:BellioMariaM | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:NobregaAlbert... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:Cardilo-ReisL... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:OliveiraAna-C... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:PeixotoJaquel... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:MedeirosMonic... | lld:pubmed |
| pubmed-article:17540734 | pubmed:author | pubmed-author:KoatzVera L... | lld:pubmed |
| pubmed-article:17540734 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17540734 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:17540734 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17540734 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17540734 | pubmed:pagination | 488-96 | lld:pubmed |
| pubmed-article:17540734 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:17540734 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17540734 | pubmed:articleTitle | Toll-like receptor 4 (TLR4)-dependent proinflammatory and immunomodulatory properties of the glycoinositolphospholipid (GIPL) from Trypanosoma cruzi. | lld:pubmed |
| pubmed-article:17540734 | pubmed:affiliation | Instituto de Microbiologia Prof. Paulo de Góes, Universidade Federal do Rio de Janeiro, CCS Bloco I, 20 andar Sala: I2-051, Avenida Carlos Chagas Filho, 373, Cidade Universitária, Ilha do Fundão, CEP: 21941-902, Rio de Janeiro, RJ, Brazil. | lld:pubmed |
| pubmed-article:17540734 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17540734 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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