<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sindhava V</submitter><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>e11445</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2897882</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5(7)</volume><pubmed_abstract>B cells are typically characterized as positive regulators of the immune response, primarily by producing antibodies. However, recent studies indicate that various subsets of B cells can perform regulatory functions mainly through IL-10 secretion. Here we discovered that peritoneal B-1 (B-1P) cells produce high levels of IL-10 upon stimulation with several Toll-like receptor (TLR) ligands. High levels of IL-10 suppressed B-1P cell proliferation and differentiation response to all TLR ligands studied in an autocrine manner in vitro and in vivo. IL-10 that accumulated in cultures inhibited B-1P cells at second and subsequent cell divisions mainly at the G1/S interphase. IL-10 inhibits TLR induced B-1P cell activation by blocking the classical NF-kappaB pathway. Co-stimulation with CD40 or BAFF abrogated the IL-10 inhibitory effect on B-1P cells during TLR stimulation. Finally, B-1P cells adoptively transferred from the peritoneal cavity of IL-10(-/-) mice showed better clearance of Borrelia hermsii than wild-type B-1P cells. This study described a novel autoregulatory property of B-1P cells mediated by B-1P cell derived IL-10, which may affect the function of B-1P cells in infection and autoimmunity.</pubmed_abstract><journal>PloS one</journal><pubmed_title>Interleukin-10 mediated autoregulation of murine B-1 B-cells and its role in Borrelia hermsii infection.</pubmed_title><pmcid>PMC2897882</pmcid><funding_grant_id>CA09357</funding_grant_id><funding_grant_id>R21 AI076956</funding_grant_id><funding_grant_id>T32 CA009357</funding_grant_id><funding_grant_id>AI076956</funding_grant_id><pubmed_authors>Bondada S</pubmed_authors><pubmed_authors>Sindhava V</pubmed_authors><pubmed_authors>Stevenson B</pubmed_authors><pubmed_authors>Woodman ME</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin-10 mediated autoregulation of murine B-1 B-cells and its role in Borrelia hermsii infection.</name><description>B cells are typically characterized as positive regulators of the immune response, primarily by producing antibodies. However, recent studies indicate that various subsets of B cells can perform regulatory functions mainly through IL-10 secretion. Here we discovered that peritoneal B-1 (B-1P) cells produce high levels of IL-10 upon stimulation with several Toll-like receptor (TLR) ligands. High levels of IL-10 suppressed B-1P cell proliferation and differentiation response to all TLR ligands studied in an autocrine manner in vitro and in vivo. IL-10 that accumulated in cultures inhibited B-1P cells at second and subsequent cell divisions mainly at the G1/S interphase. IL-10 inhibits TLR induced B-1P cell activation by blocking the classical NF-kappaB pathway. Co-stimulation with CD40 or BAFF abrogated the IL-10 inhibitory effect on B-1P cells during TLR stimulation. Finally, B-1P cells adoptively transferred from the peritoneal cavity of IL-10(-/-) mice showed better clearance of Borrelia hermsii than wild-type B-1P cells. This study described a novel autoregulatory property of B-1P cells mediated by B-1P cell derived IL-10, which may affect the function of B-1P cells in infection and autoimmunity.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Jul</publication><modification>2020-11-20T09:47:42Z</modification><creation>2019-03-26T23:08:48Z</creation></dates><accession>S-EPMC2897882</accession><cross_references><pubmed>20625435</pubmed><doi>10.1371/journal.pone.0011445</doi></cross_references></HashMap>