<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chaplin JW</submitter><funding>NIAID NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>4199-209</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3394853</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>187(8)</volume><pubmed_abstract>CD180 is homologous to TLR4 and regulates TLR4 signaling, yet its function is unclear. We report that injection of anti-CD180 mAb into mice induced rapid Ig production of all classes and subclasses, with the exception of IgA and IgG2b, with up to 50-fold increases in serum IgG1 and IgG3. IgG production after anti-CD180 injection was not due to reactivation of memory B cells and was retained in T cell-deficient (TCR knockout [KO]), CD40 KO, IL-4 KO, and MyD88 KO mice. Anti-CD180 rapidly increased both transitional and mature B cells, with especially robust increases in transitional B cell number, marginal zone B cell proliferation, and CD86, but not CD80, expression. In contrast, anti-CD40 induced primarily follicular B cell and myeloid expansion, with increases in expression of CD80 and CD</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>Anti-CD180 (RP105) activates B cells to rapidly produce polyclonal Ig via a T cell and MyD88-independent pathway.</pubmed_title><pmcid>PMC3394853</pmcid><funding_grant_id>R21 AI085311</funding_grant_id><funding_grant_id>AI44257</funding_grant_id><funding_grant_id>2T32 GM007270</funding_grant_id><funding_grant_id>AI52203</funding_grant_id><funding_grant_id>R37 AI044257</funding_grant_id><funding_grant_id>AI85311</funding_grant_id><funding_grant_id>R01 AI052203</funding_grant_id><funding_grant_id>T32 GM007270</funding_grant_id><funding_grant_id>R01 AI044257</funding_grant_id><pubmed_authors>Ledbetter JA</pubmed_authors><pubmed_authors>Kasahara S</pubmed_authors><pubmed_authors>Clark EA</pubmed_authors><pubmed_authors>Chaplin JW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Anti-CD180 (RP105) activates B cells to rapidly produce polyclonal Ig via a T cell and MyD88-independent pathway.</name><description>CD180 is homologous to TLR4 and regulates TLR4 signaling, yet its function is unclear. We report that injection of anti-CD180 mAb into mice induced rapid Ig production of all classes and subclasses, with the exception of IgA and IgG2b, with up to 50-fold increases in serum IgG1 and IgG3. IgG production after anti-CD180 injection was not due to reactivation of memory B cells and was retained in T cell-deficient (TCR knockout [KO]), CD40 KO, IL-4 KO, and MyD88 KO mice. Anti-CD180 rapidly increased both transitional and mature B cells, with especially robust increases in transitional B cell number, marginal zone B cell proliferation, and CD86, but not CD80, expression. In contrast, anti-CD40 induced primarily follicular B cell and myeloid expansion, with increases in expression of CD80 and CD</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Oct</publication><modification>2025-04-18T16:16:09.606Z</modification><creation>2019-03-27T00:55:30Z</creation></dates><accession>S-EPMC3394853</accession><cross_references><pubmed>21918197</pubmed><doi>10.4049/jimmunol.1100198</doi></cross_references></HashMap>