<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(12)</volume><submitter>Lemire P</submitter><pubmed_abstract>Group B Streptococcus (GBS) is an important agent of life-threatening invasive infection. It has been previously shown that encapsulated type III GBS is easily internalized by dendritic cells (DCs), and that this internalization had an impact on cytokine production. The receptors underlying these processes are poorly characterized. Knowledge on the mechanisms used by type V GBS to activate DCs is minimal. In this work, we investigated the role of Toll-like receptor (TLR)/MyD88 signaling pathway, the particular involvement of TLR2, and that of the intracellular sensing receptor NOD2 in the activation of DCs by types III and V GBS. The role of capsular polysaccharide (CPS, one of the most important GBS virulence factors) in bacterial-DC interactions was evaluated using non-encapsulated mutan</pubmed_abstract><journal>PloS one</journal><pagination>e113940</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4250082</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Implication of TLR- but not of NOD2-signaling pathways in dendritic cell activation by group B Streptococcus serotypes III and V.</pubmed_title><pmcid>PMC4250082</pmcid><pubmed_authors>Lemire P</pubmed_authors><pubmed_authors>Takamatsu D</pubmed_authors><pubmed_authors>Bergman E</pubmed_authors><pubmed_authors>Roy D</pubmed_authors><pubmed_authors>Segura M</pubmed_authors><pubmed_authors>Okura M</pubmed_authors><pubmed_authors>Fittipaldi N</pubmed_authors></additional><is_claimable>false</is_claimable><name>Implication of TLR- but not of NOD2-signaling pathways in dendritic cell activation by group B Streptococcus serotypes III and V.</name><description>Group B Streptococcus (GBS) is an important agent of life-threatening invasive infection. It has been previously shown that encapsulated type III GBS is easily internalized by dendritic cells (DCs), and that this internalization had an impact on cytokine production. The receptors underlying these processes are poorly characterized. Knowledge on the mechanisms used by type V GBS to activate DCs is minimal. In this work, we investigated the role of Toll-like receptor (TLR)/MyD88 signaling pathway, the particular involvement of TLR2, and that of the intracellular sensing receptor NOD2 in the activation of DCs by types III and V GBS. The role of capsular polysaccharide (CPS, one of the most important GBS virulence factors) in bacterial-DC interactions was evaluated using non-encapsulated mutan</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014</publication><modification>2025-04-22T21:54:24.639Z</modification><creation>2019-03-26T23:25:05Z</creation></dates><accession>S-EPMC4250082</accession><cross_references><pubmed>25436906</pubmed><doi>10.1371/journal.pone.0113940</doi></cross_references></HashMap>