| pubmed-article:16081774 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0018893 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0126732 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0162832 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0032594 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C1254042 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C1523987 | lld:lifeskim |
| pubmed-article:16081774 | lifeskim:mentions | umls-concept:C0332291 | lld:lifeskim |
| pubmed-article:16081774 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:16081774 | pubmed:dateCreated | 2005-8-5 | lld:pubmed |
| pubmed-article:16081774 | pubmed:abstractText | Activation of APCs via TLRs leads to activation of NF-kappaB, a key transcription factor in cells of the immune system most often associated with induction of Th1-type and proinflammatory responses. The neoglycoconjugate lacto-N-fucopentaose III (12-25 molecules)-dextran (LNFPIII-Dex) activates dendritic cells (DCs) via TLR4, as does LPS. However, unlike LPS, LNFPIII-Dex-activated cells induce Th2-type CD4+ T cell responses. This observation led us to ask whether LNFPIII-activated APCs were differentially activating NF-kappaB, and if so, could this partly account for how DCs mature in response to these two different pathogen-associated molecular patterns (PAMPs). In this study, we show that LNFPIII-Dex stimulation of APCs induces rapid, but transient NF-kappaB translocation and activity in the nucleus, in comparison with the persistent activation induced by LPS. We then demonstrate that transient vs persistent NF-kappaB activation has important implications in the development of the APC phenotype, showing that the second wave of NF-kappaB translocation in response to LPS is required for production of the proinflammatory mediator NO. In contrast to LPS, LNFPIII-stimulated APCs that only transiently activate NF-kappaB do not induce degradation of the known IkappaB family members or production of NO. However, cells stimulated with LNFPIII rapidly accumulate p50, suggesting that an alternative p105 degradation-dependent mechanism is primarily responsible for NF-kappaB activation downstream of LNFPIII. Finally, we show that while NF-kappaB translocation in LNFPIII-stimulated APCs is transient, it is required for the development of the DC 2 phenotype, confirming a crucial and multifaceted role for NF-kappaB in innate immune responses. | lld:pubmed |
| pubmed-article:16081774 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16081774 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16081774 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16081774 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16081774 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16081774 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16081774 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16081774 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16081774 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16081774 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:16081774 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16081774 | pubmed:author | pubmed-author:Da'daraAkram... | lld:pubmed |
| pubmed-article:16081774 | pubmed:author | pubmed-author:HarnDonald... | lld:pubmed |
| pubmed-article:16081774 | pubmed:author | pubmed-author:ThomasPaul... | lld:pubmed |
| pubmed-article:16081774 | pubmed:author | pubmed-author:CarterMichele... | lld:pubmed |
| pubmed-article:16081774 | pubmed:author | pubmed-author:DeSimoneTiffa... | lld:pubmed |
| pubmed-article:16081774 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16081774 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16081774 | pubmed:volume | 175 | lld:pubmed |
| pubmed-article:16081774 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16081774 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16081774 | pubmed:pagination | 2082-90 | lld:pubmed |
| pubmed-article:16081774 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:16081774 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16081774 | pubmed:articleTitle | A helminth glycan induces APC maturation via alternative NF-kappa B activation independent of I kappa B alpha degradation. | lld:pubmed |
| pubmed-article:16081774 | pubmed:affiliation | Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:16081774 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16081774 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:16081774 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16081774 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:18033 | entrezgene:pubmed | pubmed-article:16081774 | lld:entrezgene |
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