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SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation
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 infl...
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| Published in: | PloS one 2015-05, Vol.10 (5), p.e0126576 |
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| creator | Yang, Linlin Carrillo, Marykate Wu, Yuchieh M DiAngelo, Susan L Silveyra, Patricia Umstead, Todd M Halstead, E Scott Davies, Michael L Hu, Sanmei Floros, Joanna McCormack, Francis X Christensen, Neil D Chroneos, Zissis C |
| 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 negative disruption of SP-R210L augments expression of receptors including SR-A, CD14, and CD36, and enhances macrophages' inflammatory response to TLR stimulation. Finally, because SP-A is known to modulate CD14, we used a variety of techniques to investigate how SP-R210 mediates the effect of SP-A on CD14. These studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms. Together, our findings support a model in which SP-R210 isoforms differentially regulate trafficking, expression, and activation of innate immune receptors on macrophages. |
| doi_str_mv | 10.1371/journal.pone.0126576 |
| format | article |
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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 negative disruption of SP-R210L augments expression of receptors including SR-A, CD14, and CD36, and enhances macrophages' inflammatory response to TLR stimulation. Finally, because SP-A is known to modulate CD14, we used a variety of techniques to investigate how SP-R210 mediates the effect of SP-A on CD14. These studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms. Together, our findings support a model in which SP-R210 isoforms differentially regulate trafficking, expression, and activation of innate immune receptors on macrophages.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0126576</identifier><identifier>PMID: 25965346</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alternative splicing ; Alternative Splicing - genetics ; Alveoli ; Biochemistry ; CD14 antigen ; CD36 antigen ; Cell activation ; Critical care ; Cytokines ; Humans ; Immune clearance ; Immune system ; Immunity ; Immunity, Innate - genetics ; Immunology ; Inflammation ; Inflammation - chemically induced ; Inflammation - genetics ; Inflammation - immunology ; Inflammatory response ; Internalization ; Isoforms ; Kinases ; Laboratories ; Lipids ; Lipopolysaccharide Receptors - genetics ; Lipopolysaccharide Receptors - metabolism ; Lipopolysaccharides ; Lipopolysaccharides - toxicity ; Lung diseases ; Macrophages ; Macrophages, Alveolar - immunology ; Macrophages, Alveolar - metabolism ; Medical research ; Medicine ; Modulators ; Myosins - genetics ; Myosins - metabolism ; Opsonization ; Pathogens ; Pediatrics ; Phagocytosis ; Physicians ; Physiology ; Priming ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Proteins ; Pulmonary Surfactant-Associated Protein A - administration & dosage ; Pulmonary Surfactant-Associated Protein A - metabolism ; Receptors ; Surfactant protein A ; Surfactants</subject><ispartof>PloS one, 2015-05, Vol.10 (5), p.e0126576</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Yang et al 2015 Yang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-42785829989a7de91c6404c9398a396db6ab0d3752bc21a06b6b959dcd7ac2213</citedby><cites>FETCH-LOGICAL-c692t-42785829989a7de91c6404c9398a396db6ab0d3752bc21a06b6b959dcd7ac2213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1680430410/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1680430410?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,25783,27957,27958,37047,44625,53827,53829,75483</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25965346$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rottenberg, Martin E</contributor><creatorcontrib>Yang, Linlin</creatorcontrib><creatorcontrib>Carrillo, Marykate</creatorcontrib><creatorcontrib>Wu, Yuchieh M</creatorcontrib><creatorcontrib>DiAngelo, Susan L</creatorcontrib><creatorcontrib>Silveyra, Patricia</creatorcontrib><creatorcontrib>Umstead, Todd M</creatorcontrib><creatorcontrib>Halstead, E Scott</creatorcontrib><creatorcontrib>Davies, Michael L</creatorcontrib><creatorcontrib>Hu, Sanmei</creatorcontrib><creatorcontrib>Floros, Joanna</creatorcontrib><creatorcontrib>McCormack, Francis X</creatorcontrib><creatorcontrib>Christensen, Neil D</creatorcontrib><creatorcontrib>Chroneos, Zissis C</creatorcontrib><title>SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation</title><title>PloS one</title><addtitle>PLoS One</addtitle><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 negative disruption of SP-R210L augments expression of receptors including SR-A, CD14, and CD36, and enhances macrophages' inflammatory response to TLR stimulation. Finally, because SP-A is known to modulate CD14, we used a variety of techniques to investigate how SP-R210 mediates the effect of SP-A on CD14. These studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms. Together, our findings support a model in which SP-R210 isoforms differentially regulate trafficking, expression, and activation of innate immune receptors on macrophages.</description><subject>Alternative splicing</subject><subject>Alternative Splicing - genetics</subject><subject>Alveoli</subject><subject>Biochemistry</subject><subject>CD14 antigen</subject><subject>CD36 antigen</subject><subject>Cell activation</subject><subject>Critical care</subject><subject>Cytokines</subject><subject>Humans</subject><subject>Immune clearance</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunity, Innate - genetics</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammatory response</subject><subject>Internalization</subject><subject>Isoforms</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lipids</subject><subject>Lipopolysaccharide Receptors - genetics</subject><subject>Lipopolysaccharide Receptors - metabolism</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung diseases</subject><subject>Macrophages</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Modulators</subject><subject>Myosins - genetics</subject><subject>Myosins - metabolism</subject><subject>Opsonization</subject><subject>Pathogens</subject><subject>Pediatrics</subject><subject>Phagocytosis</subject><subject>Physicians</subject><subject>Physiology</subject><subject>Priming</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - metabolism</subject><subject>Proteins</subject><subject>Pulmonary Surfactant-Associated Protein A - administration & dosage</subject><subject>Pulmonary Surfactant-Associated Protein A - metabolism</subject><subject>Receptors</subject><subject>Surfactant protein A</subject><subject>Surfactants</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1rFDEUhgdRbK3-A9EBQezFrvmaZHIjLMWPhS4trfY2nEkysymzkzWZKfbfm3WnZQcUJBcJJ895c3jzZtlrjOaYCvzx1g-hg3a-9Z2dI0x4IfiT7BhLSmacIPr04HyUvYjxFqGClpw_z45IIXlBGT_Obq4vZ1cEo_zD6t7jcnGaL6OvfdjEHGK-7Prguuh0vvJmaKH3Iea-zlegg9-uobH5ZXAb1zU5dCZf6N7dQe989zJ7VkMb7atxP8l-fPn8_ezb7Pzi6_JscT7TXJJ-xogoi5JIWUoQxkqsOUNMSypLoJKbikOFDBUFqTTBgHjFK1lIo40ATQimJ9nbve629VGNlkSFeYkYRQyjRCz3hPFwq7ZpWgj3yoNTfwo-NApC73RrFddaSFvpEgtgosSVpgS0xKbg1pSWJ61P42tDtbFG22QPtBPR6U3n1qrxd4oxUgokksC7USD4n4ON_T9GHqkG0lSuq30S0xsXtVowinn6Vc4SNf8LlZaxG6dTKGqX6pOG00lDYnr7q29giFEtr6_-n724mbLvD9i1hbZfR98OuxzEKcj2YApPjMHWj85hpHaZfnBD7TKtxkyntjeHrj82PYSY_gbEZ-8k</recordid><startdate>20150512</startdate><enddate>20150512</enddate><creator>Yang, Linlin</creator><creator>Carrillo, Marykate</creator><creator>Wu, Yuchieh M</creator><creator>DiAngelo, Susan L</creator><creator>Silveyra, Patricia</creator><creator>Umstead, Todd M</creator><creator>Halstead, E Scott</creator><creator>Davies, Michael L</creator><creator>Hu, Sanmei</creator><creator>Floros, Joanna</creator><creator>McCormack, Francis X</creator><creator>Christensen, Neil D</creator><creator>Chroneos, Zissis C</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150512</creationdate><title>SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation</title><author>Yang, Linlin ; Carrillo, Marykate ; Wu, Yuchieh M ; DiAngelo, Susan L ; Silveyra, Patricia ; Umstead, Todd M ; Halstead, E Scott ; Davies, Michael L ; Hu, Sanmei ; Floros, Joanna ; McCormack, Francis X ; Christensen, Neil D ; Chroneos, Zissis C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-42785829989a7de91c6404c9398a396db6ab0d3752bc21a06b6b959dcd7ac2213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alternative splicing</topic><topic>Alternative Splicing - genetics</topic><topic>Alveoli</topic><topic>Biochemistry</topic><topic>CD14 antigen</topic><topic>CD36 antigen</topic><topic>Cell activation</topic><topic>Critical care</topic><topic>Cytokines</topic><topic>Humans</topic><topic>Immune clearance</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunity, Innate - genetics</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammatory response</topic><topic>Internalization</topic><topic>Isoforms</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Lipids</topic><topic>Lipopolysaccharide Receptors - genetics</topic><topic>Lipopolysaccharide Receptors - metabolism</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung diseases</topic><topic>Macrophages</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Modulators</topic><topic>Myosins - genetics</topic><topic>Myosins - metabolism</topic><topic>Opsonization</topic><topic>Pathogens</topic><topic>Pediatrics</topic><topic>Phagocytosis</topic><topic>Physicians</topic><topic>Physiology</topic><topic>Priming</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - metabolism</topic><topic>Proteins</topic><topic>Pulmonary Surfactant-Associated Protein A - administration & dosage</topic><topic>Pulmonary Surfactant-Associated Protein A - metabolism</topic><topic>Receptors</topic><topic>Surfactant protein A</topic><topic>Surfactants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Linlin</creatorcontrib><creatorcontrib>Carrillo, Marykate</creatorcontrib><creatorcontrib>Wu, Yuchieh M</creatorcontrib><creatorcontrib>DiAngelo, Susan L</creatorcontrib><creatorcontrib>Silveyra, Patricia</creatorcontrib><creatorcontrib>Umstead, Todd M</creatorcontrib><creatorcontrib>Halstead, E Scott</creatorcontrib><creatorcontrib>Davies, Michael L</creatorcontrib><creatorcontrib>Hu, Sanmei</creatorcontrib><creatorcontrib>Floros, Joanna</creatorcontrib><creatorcontrib>McCormack, Francis X</creatorcontrib><creatorcontrib>Christensen, Neil D</creatorcontrib><creatorcontrib>Chroneos, Zissis C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale in Context : Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - 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Performed the experiments: YMW SLD PS TMU ESH LY SH MLD ZCC. Analyzed the data: ZCC YMW PS TMU LY. Contributed reagents/materials/analysis tools: ZCC JF PS NDC FXM. Wrote the paper: ZCC. Critical manuscript reading: ZCC JF ESH TMU PS YMW NDC MLD MC LY.</notes><notes>Competing Interests: The authors have declared that no competing interests exist.</notes><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 negative disruption of SP-R210L augments expression of receptors including SR-A, CD14, and CD36, and enhances macrophages' inflammatory response to TLR stimulation. Finally, because SP-A is known to modulate CD14, we used a variety of techniques to investigate how SP-R210 mediates the effect of SP-A on CD14. These studies revealed a novel physical association between SP-R210S, CD14, and SR-A leading to an enhanced response to LPS, and found that SP-R210L and SP-R210S regulate internalization of CD14 via distinct macropinocytosis-like mechanisms. Together, our findings support a model in which SP-R210 isoforms differentially regulate trafficking, expression, and activation of innate immune receptors on macrophages.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25965346</pmid><doi>10.1371/journal.pone.0126576</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2015-05, Vol.10 (5), p.e0126576 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1680430410 |
| source | Publicly Available Content Database; PubMed Central |
| subjects | Alternative splicing Alternative Splicing - genetics Alveoli Biochemistry CD14 antigen CD36 antigen Cell activation Critical care Cytokines Humans Immune clearance Immune system Immunity Immunity, Innate - genetics Immunology Inflammation Inflammation - chemically induced Inflammation - genetics Inflammation - immunology Inflammatory response Internalization Isoforms Kinases Laboratories Lipids Lipopolysaccharide Receptors - genetics Lipopolysaccharide Receptors - metabolism Lipopolysaccharides Lipopolysaccharides - toxicity Lung diseases Macrophages Macrophages, Alveolar - immunology Macrophages, Alveolar - metabolism Medical research Medicine Modulators Myosins - genetics Myosins - metabolism Opsonization Pathogens Pediatrics Phagocytosis Physicians Physiology Priming Protein Isoforms - genetics Protein Isoforms - metabolism Proteins Pulmonary Surfactant-Associated Protein A - administration & dosage Pulmonary Surfactant-Associated Protein A - metabolism Receptors Surfactant protein A Surfactants |
| title | SP-R210 (Myo18A) Isoforms as Intrinsic Modulators of Macrophage Priming and Activation |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-09-22T21%3A20%3A39IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=SP-R210%20(Myo18A)%20Isoforms%20as%20Intrinsic%20Modulators%20of%20Macrophage%20Priming%20and%20Activation&rft.jtitle=PloS%20one&rft.au=Yang,%20Linlin&rft.date=2015-05-12&rft.volume=10&rft.issue=5&rft.spage=e0126576&rft.pages=e0126576-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0126576&rft_dat=%3Cgale_plos_%3EA431693264%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c692t-42785829989a7de91c6404c9398a396db6ab0d3752bc21a06b6b959dcd7ac2213%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1680430410&rft_id=info:pmid/25965346&rft_galeid=A431693264&rfr_iscdi=true |