<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rauch PJ</submitter><funding>NCRR NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>PHS HHS</funding><pagination>597-601</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3279743</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>335(6068)</volume><pubmed_abstract>Recognition and clearance of a bacterial infection are a fundamental properties of innate immunity. Here, we describe an effector B cell population that protects against microbial sepsis. Innate response activator (IRA) B cells are phenotypically and functionally distinct, develop and diverge from B1a B cells, depend on pattern-recognition receptors, and produce granulocyte-macrophage colony-stimulating factor. Specific deletion of IRA B cell activity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock. These observations enrich our understanding of innate immunity, position IRA B cells as gatekeepers of bacterial infection, and identify new treatment avenues for infectious diseases.</pubmed_abstract><journal>Science (New York, N.Y.)</journal><pubmed_title>Innate response activator B cells protect against microbial sepsis.</pubmed_title><pmcid>PMC3279743</pmcid><funding_grant_id>P50 CA086355-11</funding_grant_id><funding_grant_id>R24 CA69246</funding_grant_id><funding_grant_id>1R01HL095612</funding_grant_id><funding_grant_id>P50 CA086355</funding_grant_id><funding_grant_id>P50 CA86355</funding_grant_id><funding_grant_id>P01-A154904</funding_grant_id><funding_grant_id>S10 RR026360</funding_grant_id><funding_grant_id>U01 HL080731</funding_grant_id><funding_grant_id>R01 HL095612</funding_grant_id><funding_grant_id>R01 HL095612-03</funding_grant_id><funding_grant_id>U01 HL080731-04</funding_grant_id><funding_grant_id>P01 CA069246</funding_grant_id><pubmed_authors>Etzrodt M</pubmed_authors><pubmed_authors>Nahrendorf M</pubmed_authors><pubmed_authors>Weber GF</pubmed_authors><pubmed_authors>Weissleder R</pubmed_authors><pubmed_authors>Robbins CS</pubmed_authors><pubmed_authors>Rauch PJ</pubmed_authors><pubmed_authors>Waring MT</pubmed_authors><pubmed_authors>Chudnovskiy A</pubmed_authors><pubmed_authors>Theurl I</pubmed_authors><pubmed_authors>Hilgendorf I</pubmed_authors><pubmed_authors>Chicoine AT</pubmed_authors><pubmed_authors>Pittet MJ</pubmed_authors><pubmed_authors>Swirski FK</pubmed_authors><pubmed_authors>Gorbatov R</pubmed_authors><pubmed_authors>Iwamoto Y</pubmed_authors><pubmed_authors>Mouded M</pubmed_authors><pubmed_authors>Figueiredo JL</pubmed_authors><pubmed_authors>Tiglao E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Innate response activator B cells protect against microbial sepsis.</name><description>Recognition and clearance of a bacterial infection are a fundamental properties of innate immunity. Here, we describe an effector B cell population that protects against microbial sepsis. Innate response activator (IRA) B cells are phenotypically and functionally distinct, develop and diverge from B1a B cells, depend on pattern-recognition receptors, and produce granulocyte-macrophage colony-stimulating factor. Specific deletion of IRA B cell activity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock. These observations enrich our understanding of innate immunity, position IRA B cells as gatekeepers of bacterial infection, and identify new treatment avenues for infectious diseases.</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Feb</publication><modification>2020-11-07T08:41:02Z</modification><creation>2019-03-27T00:49:10Z</creation></dates><accession>S-EPMC3279743</accession><cross_references><pubmed>22245738</pubmed><doi>10.1126/science.1215173</doi></cross_references></HashMap>