A Lectin-EGF antibody promotes regulatory T cells and attenuates nephrotoxic nephritis via DC-SIGN on dendritic cells
Interactions between dendritic cells (DCs) and T cells play a critical role in the development of glomerulonephritis, which is a common cause of chronic kidney disease. DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), an immune-regulating molecule of the C-type lectin f...
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| Veröffentlicht in: | Journal of translational medicine 2013-04, Vol.11 (1), p.103-103, Article 103 |
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| creator | Cai, Minchao Wu, Jing Mao, Chaoming Ren, Jianmin Li, Pu Li, Xiao Zhong, Jiuchang Xu, Chundi Zhou, Tong |
| description | Interactions between dendritic cells (DCs) and T cells play a critical role in the development of glomerulonephritis, which is a common cause of chronic kidney disease. DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), an immune-regulating molecule of the C-type lectin family, is mainly expressed on DCs and mediates DC adhesion and migration, inflammation, activation of primary T cells. DC-SIGN triggers immune responses and is involved in the immune escape of pathogens and tumours. In addition, ligation of DC-SIGN on DCs actively primes DCs to induce Tregs. Under certain conditions, DC-SIGN signalling may result in inhibition of DC maturation, by promoting regulatory T cell (Treg) function and affecting Th1/Th2 bias.
A rat model of nephrotoxic nephritis was used to investigate the therapeutic effects of an anti-lectin-epidermal growth factor (EGF) antibody on glomerulonephritis. DCs were induced by human peripheral blood mononuclear cells in vitro. The expression of DC surface antigens were detected using flow cytometry; the levels of cytokines were detected by ELISA and qPCR, respectively; the capability of DCs to stimulate T cell proliferation was examined by mixed lymphocyte reaction; PsL-EGFmAb targeting to DC-SIGN on DCs was identified by immunoprecipitation.
Anti-Lectin-EGF antibody significantly reduced global crescent formation, tubulointerstitial injury and improved renal function impairment through inhibiting DC maturation and modulating Foxp3 expression and the Th1/Th2 cytokine balance in kidney. Binding of anti-Lectin-EGF antibody to DC-SIGN on human DCs inhibited DC maturation, increased IL-10 production from DCs and enhanced CD4+CD25+ Treg functions.
Our results suggest that treatment with anti-Lectin-EGF antibody modulates DCs to suppressive DCs and enhances Treg functions, contributing to the attenuation of renal injury in a rat model of nephrotoxic nephritis. |
| doi_str_mv | 10.1186/1479-5876-11-103 |
| format | Article |
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A rat model of nephrotoxic nephritis was used to investigate the therapeutic effects of an anti-lectin-epidermal growth factor (EGF) antibody on glomerulonephritis. DCs were induced by human peripheral blood mononuclear cells in vitro. The expression of DC surface antigens were detected using flow cytometry; the levels of cytokines were detected by ELISA and qPCR, respectively; the capability of DCs to stimulate T cell proliferation was examined by mixed lymphocyte reaction; PsL-EGFmAb targeting to DC-SIGN on DCs was identified by immunoprecipitation.
Anti-Lectin-EGF antibody significantly reduced global crescent formation, tubulointerstitial injury and improved renal function impairment through inhibiting DC maturation and modulating Foxp3 expression and the Th1/Th2 cytokine balance in kidney. Binding of anti-Lectin-EGF antibody to DC-SIGN on human DCs inhibited DC maturation, increased IL-10 production from DCs and enhanced CD4+CD25+ Treg functions.
Our results suggest that treatment with anti-Lectin-EGF antibody modulates DCs to suppressive DCs and enhances Treg functions, contributing to the attenuation of renal injury in a rat model of nephrotoxic nephritis.</description><identifier>ISSN: 1479-5876</identifier><identifier>EISSN: 1479-5876</identifier><identifier>DOI: 10.1186/1479-5876-11-103</identifier><identifier>PMID: 23627732</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Acquisitions & mergers ; Animals ; Antibodies - chemistry ; Antibodies, Monoclonal - chemistry ; Antigens, Surface - metabolism ; Care and treatment ; CD4-Positive T-Lymphocytes - cytology ; Cell Adhesion Molecules - metabolism ; Chronic kidney failure ; Dendritic cells ; Dendritic Cells - cytology ; Diagnosis ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Epidermal growth factor ; Epidermal Growth Factor - chemistry ; Health sciences ; Hospitals ; Humans ; Immune response ; Immunity ; Inflammation ; Interleukin-2 Receptor alpha Subunit - metabolism ; Kidney - injuries ; Kidneys ; Lectins, C-Type - metabolism ; Lymphocytes ; Male ; Medicine ; Nephritis - metabolism ; Nitrogen ; Physiological aspects ; Protein Structure, Tertiary ; Proteins ; Rats ; Rats, Inbred WKY ; Receptors, Cell Surface - metabolism ; Regulation ; Renal Insufficiency, Chronic - metabolism ; Rodents ; Signal Transduction ; T cells ; T-Lymphocytes, Regulatory - cytology ; Th1 Cells - cytology ; Th2 Cells - cytology</subject><ispartof>Journal of translational medicine, 2013-04, Vol.11 (1), p.103-103, Article 103</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Cai et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Cai et al.; licensee BioMed Central Ltd. 2013 Cai et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b584t-626655c957d4fa99e282030f60e600f98ca2dac5d55f9affb1d996b1cfea6f713</citedby><cites>FETCH-LOGICAL-b584t-626655c957d4fa99e282030f60e600f98ca2dac5d55f9affb1d996b1cfea6f713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651349/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651349/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23627732$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cai, Minchao</creatorcontrib><creatorcontrib>Wu, Jing</creatorcontrib><creatorcontrib>Mao, Chaoming</creatorcontrib><creatorcontrib>Ren, Jianmin</creatorcontrib><creatorcontrib>Li, Pu</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Zhong, Jiuchang</creatorcontrib><creatorcontrib>Xu, Chundi</creatorcontrib><creatorcontrib>Zhou, Tong</creatorcontrib><title>A Lectin-EGF antibody promotes regulatory T cells and attenuates nephrotoxic nephritis via DC-SIGN on dendritic cells</title><title>Journal of translational medicine</title><addtitle>J Transl Med</addtitle><description>Interactions between dendritic cells (DCs) and T cells play a critical role in the development of glomerulonephritis, which is a common cause of chronic kidney disease. DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), an immune-regulating molecule of the C-type lectin family, is mainly expressed on DCs and mediates DC adhesion and migration, inflammation, activation of primary T cells. DC-SIGN triggers immune responses and is involved in the immune escape of pathogens and tumours. In addition, ligation of DC-SIGN on DCs actively primes DCs to induce Tregs. Under certain conditions, DC-SIGN signalling may result in inhibition of DC maturation, by promoting regulatory T cell (Treg) function and affecting Th1/Th2 bias.
A rat model of nephrotoxic nephritis was used to investigate the therapeutic effects of an anti-lectin-epidermal growth factor (EGF) antibody on glomerulonephritis. DCs were induced by human peripheral blood mononuclear cells in vitro. The expression of DC surface antigens were detected using flow cytometry; the levels of cytokines were detected by ELISA and qPCR, respectively; the capability of DCs to stimulate T cell proliferation was examined by mixed lymphocyte reaction; PsL-EGFmAb targeting to DC-SIGN on DCs was identified by immunoprecipitation.
Anti-Lectin-EGF antibody significantly reduced global crescent formation, tubulointerstitial injury and improved renal function impairment through inhibiting DC maturation and modulating Foxp3 expression and the Th1/Th2 cytokine balance in kidney. Binding of anti-Lectin-EGF antibody to DC-SIGN on human DCs inhibited DC maturation, increased IL-10 production from DCs and enhanced CD4+CD25+ Treg functions.
Our results suggest that treatment with anti-Lectin-EGF antibody modulates DCs to suppressive DCs and enhances Treg functions, contributing to the attenuation of renal injury in a rat model of nephrotoxic nephritis.</description><subject>Acquisitions & mergers</subject><subject>Animals</subject><subject>Antibodies - chemistry</subject><subject>Antibodies, Monoclonal - chemistry</subject><subject>Antigens, Surface - metabolism</subject><subject>Care and treatment</subject><subject>CD4-Positive T-Lymphocytes - cytology</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Chronic kidney failure</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - cytology</subject><subject>Diagnosis</subject><subject>Disease Models, Animal</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - chemistry</subject><subject>Health sciences</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunity</subject><subject>Inflammation</subject><subject>Interleukin-2 Receptor alpha Subunit - metabolism</subject><subject>Kidney - injuries</subject><subject>Kidneys</subject><subject>Lectins, C-Type - metabolism</subject><subject>Lymphocytes</subject><subject>Male</subject><subject>Medicine</subject><subject>Nephritis - metabolism</subject><subject>Nitrogen</subject><subject>Physiological aspects</subject><subject>Protein Structure, Tertiary</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Inbred WKY</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Regulation</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>T cells</subject><subject>T-Lymphocytes, Regulatory - cytology</subject><subject>Th1 Cells - cytology</subject><subject>Th2 Cells - cytology</subject><issn>1479-5876</issn><issn>1479-5876</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1Uk1v1DAQjRCIfsCdE7LEhUuKHcd2fEFaLe1SaQUHytly_LF1ldiL7VTsv8fRtksXFfng0bw3bzzPU1XvELxAqKOfUMt4TTpGa4RqBPGL6vSQevkkPqnOUrqDsGlJy19XJw2mDWO4Oa2mBVgblZ2vL1dXQPrs-qB3YBvDGLJJIJrNNMgc4g7cAGWGIRWSBjJn4yc5M7zZ3saQw2-n9rHLLoF7J8GXZf3jevUNBA-08XoG1F7jTfXKyiGZtw_3efXz6vJm-bVef19dLxfruiddm2vaUEqI4oTp1krOTdM1EENLoaEQWt4p2WipiCbEcmltjzTntEfKGkktQ_i8-rzX3U79aLQyPkc5iG10o4w7EaQTx4h3t2IT7gWmBOGWF4HlXqB34T8Cx4gKo5htF7PtAiFRfqWofHx4Rgy_JpOyGF2ajZDehCkJhClrO8Y6Wqgf_qHehSn6YlJhEQwRo7T7y9rIwQjnbSjN1SwqFgS3lHGM5rYXz7DK0WZ0KnhjXckfFcB9gYohpWjsYVAExbxwz432_qnDh4LHDcN_AITS0Sw</recordid><startdate>20130429</startdate><enddate>20130429</enddate><creator>Cai, Minchao</creator><creator>Wu, Jing</creator><creator>Mao, Chaoming</creator><creator>Ren, Jianmin</creator><creator>Li, Pu</creator><creator>Li, Xiao</creator><creator>Zhong, Jiuchang</creator><creator>Xu, Chundi</creator><creator>Zhou, Tong</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20130429</creationdate><title>A Lectin-EGF antibody promotes regulatory T cells and attenuates nephrotoxic nephritis via DC-SIGN on dendritic cells</title><author>Cai, Minchao ; Wu, Jing ; Mao, Chaoming ; Ren, Jianmin ; Li, Pu ; Li, Xiao ; Zhong, Jiuchang ; Xu, Chundi ; Zhou, Tong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b584t-626655c957d4fa99e282030f60e600f98ca2dac5d55f9affb1d996b1cfea6f713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acquisitions & mergers</topic><topic>Animals</topic><topic>Antibodies - chemistry</topic><topic>Antibodies, Monoclonal - chemistry</topic><topic>Antigens, Surface - metabolism</topic><topic>Care and treatment</topic><topic>CD4-Positive T-Lymphocytes - cytology</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Chronic kidney failure</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - cytology</topic><topic>Diagnosis</topic><topic>Disease Models, Animal</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - chemistry</topic><topic>Health sciences</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunity</topic><topic>Inflammation</topic><topic>Interleukin-2 Receptor alpha Subunit - metabolism</topic><topic>Kidney - injuries</topic><topic>Kidneys</topic><topic>Lectins, C-Type - metabolism</topic><topic>Lymphocytes</topic><topic>Male</topic><topic>Medicine</topic><topic>Nephritis - metabolism</topic><topic>Nitrogen</topic><topic>Physiological aspects</topic><topic>Protein Structure, Tertiary</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Inbred WKY</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Regulation</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>T cells</topic><topic>T-Lymphocytes, Regulatory - cytology</topic><topic>Th1 Cells - cytology</topic><topic>Th2 Cells - cytology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cai, Minchao</creatorcontrib><creatorcontrib>Wu, Jing</creatorcontrib><creatorcontrib>Mao, Chaoming</creatorcontrib><creatorcontrib>Ren, Jianmin</creatorcontrib><creatorcontrib>Li, Pu</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Zhong, Jiuchang</creatorcontrib><creatorcontrib>Xu, Chundi</creatorcontrib><creatorcontrib>Zhou, Tong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of translational medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cai, Minchao</au><au>Wu, Jing</au><au>Mao, Chaoming</au><au>Ren, Jianmin</au><au>Li, Pu</au><au>Li, Xiao</au><au>Zhong, Jiuchang</au><au>Xu, Chundi</au><au>Zhou, Tong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Lectin-EGF antibody promotes regulatory T cells and attenuates nephrotoxic nephritis via DC-SIGN on dendritic cells</atitle><jtitle>Journal of translational medicine</jtitle><addtitle>J Transl Med</addtitle><date>2013-04-29</date><risdate>2013</risdate><volume>11</volume><issue>1</issue><spage>103</spage><epage>103</epage><pages>103-103</pages><artnum>103</artnum><issn>1479-5876</issn><eissn>1479-5876</eissn><abstract>Interactions between dendritic cells (DCs) and T cells play a critical role in the development of glomerulonephritis, which is a common cause of chronic kidney disease. DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), an immune-regulating molecule of the C-type lectin family, is mainly expressed on DCs and mediates DC adhesion and migration, inflammation, activation of primary T cells. DC-SIGN triggers immune responses and is involved in the immune escape of pathogens and tumours. In addition, ligation of DC-SIGN on DCs actively primes DCs to induce Tregs. Under certain conditions, DC-SIGN signalling may result in inhibition of DC maturation, by promoting regulatory T cell (Treg) function and affecting Th1/Th2 bias.
A rat model of nephrotoxic nephritis was used to investigate the therapeutic effects of an anti-lectin-epidermal growth factor (EGF) antibody on glomerulonephritis. DCs were induced by human peripheral blood mononuclear cells in vitro. The expression of DC surface antigens were detected using flow cytometry; the levels of cytokines were detected by ELISA and qPCR, respectively; the capability of DCs to stimulate T cell proliferation was examined by mixed lymphocyte reaction; PsL-EGFmAb targeting to DC-SIGN on DCs was identified by immunoprecipitation.
Anti-Lectin-EGF antibody significantly reduced global crescent formation, tubulointerstitial injury and improved renal function impairment through inhibiting DC maturation and modulating Foxp3 expression and the Th1/Th2 cytokine balance in kidney. Binding of anti-Lectin-EGF antibody to DC-SIGN on human DCs inhibited DC maturation, increased IL-10 production from DCs and enhanced CD4+CD25+ Treg functions.
Our results suggest that treatment with anti-Lectin-EGF antibody modulates DCs to suppressive DCs and enhances Treg functions, contributing to the attenuation of renal injury in a rat model of nephrotoxic nephritis.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23627732</pmid><doi>10.1186/1479-5876-11-103</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acquisitions & mergers Animals Antibodies - chemistry Antibodies, Monoclonal - chemistry Antigens, Surface - metabolism Care and treatment CD4-Positive T-Lymphocytes - cytology Cell Adhesion Molecules - metabolism Chronic kidney failure Dendritic cells Dendritic Cells - cytology Diagnosis Disease Models, Animal Enzyme-Linked Immunosorbent Assay Epidermal growth factor Epidermal Growth Factor - chemistry Health sciences Hospitals Humans Immune response Immunity Inflammation Interleukin-2 Receptor alpha Subunit - metabolism Kidney - injuries Kidneys Lectins, C-Type - metabolism Lymphocytes Male Medicine Nephritis - metabolism Nitrogen Physiological aspects Protein Structure, Tertiary Proteins Rats Rats, Inbred WKY Receptors, Cell Surface - metabolism Regulation Renal Insufficiency, Chronic - metabolism Rodents Signal Transduction T cells T-Lymphocytes, Regulatory - cytology Th1 Cells - cytology Th2 Cells - cytology |
| title | A Lectin-EGF antibody promotes regulatory T cells and attenuates nephrotoxic nephritis via DC-SIGN on dendritic cells |
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