<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cunningham AL</submitter><funding>NIAID NIH HHS</funding><funding>National Center on Minority Health and Health Disparities</funding><funding>NIMHD NIH HHS</funding><funding>U.S. Department of Defense</funding><funding>National Institutes of Health</funding><pagination>e0153402</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4839702</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(4)</volume><pubmed_abstract>M-cells (microfold cells) are thought to be a primary conduit of intestinal antigen trafficking. Using an established neutralizing anti-RANKL (Receptor Activator of NF-κB Ligand) antibody treatment to transiently deplete M-cells in vivo, we sought to determine whether intestinal M-cells were required for the effective induction of protective immunity following oral vaccination with ΔiglB (a defined live attenuated Francisella novicida mutant). M-cell depleted, ΔiglB-vaccinated mice exhibited increased (but not significant) morbidity and mortality following a subsequent homotypic or heterotypic pulmonary F. tularensis challenge. No significant differences in splenic IFN-γ, IL-2, or IL-17 or serum antibody (IgG1, IgG2a, IgA) production were observed compared to non-depleted, ΔiglB-vaccinated</pubmed_abstract><journal>PloS one</journal><pubmed_title>M-Cells Contribute to the Entry of an Oral Vaccine but Are Not Essential for the Subsequent Induction of Protective Immunity against Francisella tularensis.</pubmed_title><pmcid>PMC4839702</pmcid><funding_grant_id>T32AI007271</funding_grant_id><funding_grant_id>T32 AI007271</funding_grant_id><funding_grant_id>G12MD007591</funding_grant_id><funding_grant_id>W911NF-11-1-0136</funding_grant_id><funding_grant_id>R21 AI114762</funding_grant_id><funding_grant_id>G12 MD007591</funding_grant_id><pubmed_authors>Cunningham AL</pubmed_authors><pubmed_authors>Hung CY</pubmed_authors><pubmed_authors>Williams IR</pubmed_authors><pubmed_authors>Navara CS</pubmed_authors><pubmed_authors>Yagita H</pubmed_authors><pubmed_authors>Eaves-Pyles TD</pubmed_authors><pubmed_authors>Klose KE</pubmed_authors><pubmed_authors>Arulanandam BP</pubmed_authors><pubmed_authors>Guentzel MN</pubmed_authors><pubmed_authors>Yu JJ</pubmed_authors><pubmed_authors>Forsthuber TG</pubmed_authors></additional><is_claimable>false</is_claimable><name>M-Cells Contribute to the Entry of an Oral Vaccine but Are Not Essential for the Subsequent Induction of Protective Immunity against Francisella tularensis.</name><description>M-cells (microfold cells) are thought to be a primary conduit of intestinal antigen trafficking. Using an established neutralizing anti-RANKL (Receptor Activator of NF-κB Ligand) antibody treatment to transiently deplete M-cells in vivo, we sought to determine whether intestinal M-cells were required for the effective induction of protective immunity following oral vaccination with ΔiglB (a defined live attenuated Francisella novicida mutant). M-cell depleted, ΔiglB-vaccinated mice exhibited increased (but not significant) morbidity and mortality following a subsequent homotypic or heterotypic pulmonary F. tularensis challenge. No significant differences in splenic IFN-γ, IL-2, or IL-17 or serum antibody (IgG1, IgG2a, IgA) production were observed compared to non-depleted, ΔiglB-vaccinated</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016</publication><modification>2025-04-19T14:01:02.691Z</modification><creation>2019-03-26T22:53:50Z</creation></dates><accession>S-EPMC4839702</accession><cross_references><pubmed>27100824</pubmed><doi>10.1371/journal.pone.0153402</doi></cross_references></HashMap>