<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang L</submitter><funding>NICHD NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>e0126576</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4428707</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(5)</volume><pubmed_abstract>The surfactant protein (SP-A) receptor SP-R210 has been shown to increase phagocytosis of SP-A-bound pathogens and to modulate cytokine secretion by immune cells. SP-A plays an important role in pulmonary immunity by enhancing opsonization and clearance of pathogens and by modulating macrophage inflammatory responses. Alternative splicing of the Myo18A gene results in two isoforms: SP-R210S and SP-R210L, with the latter predominantly expressed in alveolar macrophages. In this study we show that SP-A is required for optimal expression of SP-R210L on alveolar macrophages. Interestingly, pre-treatment with SP-A prepared by different methods either enhances or suppresses responsiveness to LPS, possibly due to differential co-isolation of SP-B or other proteins. We also report that dominant neg</pubmed_abstract><journal>PloS one</journal><pubmed_title>SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation.</pubmed_title><pmcid>PMC4428707</pmcid><funding_grant_id>HL068127</funding_grant_id><funding_grant_id>HL-34788</funding_grant_id><funding_grant_id>K12 HD055882</funding_grant_id><funding_grant_id>R01 HL034788</funding_grant_id><funding_grant_id>R01 HL068127</funding_grant_id><funding_grant_id>R37 HL034788</funding_grant_id><pubmed_authors>Floros J</pubmed_authors><pubmed_authors>Hu S</pubmed_authors><pubmed_authors>Yang L</pubmed_authors><pubmed_authors>Silveyra P</pubmed_authors><pubmed_authors>DiAngelo SL</pubmed_authors><pubmed_authors>Halstead ES</pubmed_authors><pubmed_authors>Chroneos ZC</pubmed_authors><pubmed_authors>Wu YM</pubmed_authors><pubmed_authors>Davies ML</pubmed_authors><pubmed_authors>Christensen ND</pubmed_authors><pubmed_authors>Umstead TM</pubmed_authors><pubmed_authors>Carrillo M</pubmed_authors><pubmed_authors>McCormack FX</pubmed_authors></additional><is_claimable>false</is_claimable><name>SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation.</name><description>The surfactant protein (SP-A) receptor SP-R210 has been shown to increase phagocytosis of SP-A-bound pathogens and to modulate cytokine secretion by immune cells. SP-A plays an important role in pulmonary immunity by enhancing opsonization and clearance of pathogens and by modulating macrophage inflammatory responses. Alternative splicing of the Myo18A gene results in two isoforms: SP-R210S and SP-R210L, with the latter predominantly expressed in alveolar macrophages. In this study we show that SP-A is required for optimal expression of SP-R210L on alveolar macrophages. Interestingly, pre-treatment with SP-A prepared by different methods either enhances or suppresses responsiveness to LPS, possibly due to differential co-isolation of SP-B or other proteins. We also report that dominant neg</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2025-04-22T07:09:00.803Z</modification><creation>2019-03-26T23:32:41Z</creation></dates><accession>S-EPMC4428707</accession><cross_references><pubmed>25965346</pubmed><doi>10.1371/journal.pone.0126576</doi></cross_references></HashMap>