The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis
Background. Blockade of CD40–CD40 ligand (CD154) interactions protects against renal injury in adriamycin nephropathy (AN) in immunocompetent mice. To investigate whether this protection relied on adaptive or cognate immunity, we tested the effect of CD40–CD154 blockade in severe combined immunodefi...
Gespeichert in:
| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2010-03, Vol.25 (3), p.717-730 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 730 |
|---|---|
| container_issue | 3 |
| container_start_page | 717 |
| container_title | Nephrology, dialysis, transplantation |
| container_volume | 25 |
| creator | Lee, Vincent W.S. Qin, Xiaohong Wang, Yiping Zheng, Guoping Wang, Ya Wang, Ying Ince, Jon Tan, Thian K. Kairaitis, Lukas K. Alexander, Stephen I. Harris, David C.H. |
| description | Background. Blockade of CD40–CD40 ligand (CD154) interactions protects against renal injury in adriamycin nephropathy (AN) in immunocompetent mice. To investigate whether this protection relied on adaptive or cognate immunity, we tested the effect of CD40–CD154 blockade in severe combined immunodeficient (SCID) mice. Methods. SCID mice were divided into three groups: normal, AN + hamster IgG (ADR+IgG group) and AN + anti-CD154 antibody (MR1) (ADR+MR1 group). AN was induced by tail vein injection of 5.2 mg/kg of adriamycin (ADR). Hamster IgG (control Ab) or MR1 was administered intraperitoneally on days 5, 7, 9 and 11 after ADR injection. Histological and functional data were collected 4 weeks after ADR injection. In vitro experiments tested the effect of soluble and cell-bound CD154 co-cultured with CD40-expressing cells [macrophages, mesangial cells and renal tubular epithelial cells (RTEC)]. Results. All experimental animals developed nephropathy. Compared to the ADR+IgG group, ADR+MR1 animals had significantly less histological injury (glomerulosclerosis and tubular atrophy) and functional injury (creatinine clearance). Kidneys of ADR+MR1 animals had significantly less macrophage infiltration than those of ADR+IgG animals. Interestingly, expression of CD40 and CD41 (a platelet-specific marker) was significantly less in ADR+MR1 animals compared to ADR+IgG animals. In vitro, CD154 blockade significantly attenuated upregulation of CCL2 gene expression by RTEC stimulated by activated macrophage-conditioned medium. In contrast, platelet-induced upregulation of macrophage and mesangial cell proinflammatory cytokine gene expression were not CD154-dependent. Conclusion. CD40–CD154 blockade has a significant innate renoprotective effect in ADR nephrosis. This is potentially due to inhibition of macrophage-derived soluble CD154. |
| doi_str_mv | 10.1093/ndt/gfp569 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_746086620</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ndt/gfp569</oup_id><sourcerecordid>746086620</sourcerecordid><originalsourceid>FETCH-LOGICAL-c452t-7a17a66c5d1a102654d6e67e40697e74cb96663ac68357f2e6ddeb08d59a5c873</originalsourceid><addsrcrecordid>eNqFkMtKHEEUhgtJ0HHiJg8QehMCQmtdum7LMCZRMWShERGkOFNdnSnTXd2p6iaZXd4hb5gnscIMuour_8D5-A_nQ-g1wUcEa3Yc6vH4WzNwoXfQjFQCl5Qp_gLN8pKUmGO9h_ZTuscYayrlLtojWimtJJuhu6uVKxYnFf77-8_ihPCqsH2ZRt9NLYy-D8UA4-onrIvO1R5GlwofQs7Cd90UcoT7Ka5zFFBHD93a5jG4YRX75NMr9LKBNrmDbc7R148frhan5cWXT2eL9xelrTgdSwlEghCW1wQIpoJXtXBCugoLLZ2s7FILIRhYoRiXDXWirt0Sq5pr4Db_MUfvNr1D7H9MLo2m88m6toXg-ikZmaUoISh-nmSMMCqzuTk63JA2v5Kia8wQfQdxbQg2_7yb7N1svGf4zbZ2WmZTT-hWdAbebgFIFtomQrA-PXKUCoV5pZ64fhr-f7DccD6N7tcjCfG7EZJJbk5vbo3-zPWlvr415-wBxJqn0g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>733132709</pqid></control><display><type>article</type><title>The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Lee, Vincent W.S. ; Qin, Xiaohong ; Wang, Yiping ; Zheng, Guoping ; Wang, Ya ; Wang, Ying ; Ince, Jon ; Tan, Thian K. ; Kairaitis, Lukas K. ; Alexander, Stephen I. ; Harris, David C.H.</creator><creatorcontrib>Lee, Vincent W.S. ; Qin, Xiaohong ; Wang, Yiping ; Zheng, Guoping ; Wang, Ya ; Wang, Ying ; Ince, Jon ; Tan, Thian K. ; Kairaitis, Lukas K. ; Alexander, Stephen I. ; Harris, David C.H.</creatorcontrib><description>Background. Blockade of CD40–CD40 ligand (CD154) interactions protects against renal injury in adriamycin nephropathy (AN) in immunocompetent mice. To investigate whether this protection relied on adaptive or cognate immunity, we tested the effect of CD40–CD154 blockade in severe combined immunodeficient (SCID) mice. Methods. SCID mice were divided into three groups: normal, AN + hamster IgG (ADR+IgG group) and AN + anti-CD154 antibody (MR1) (ADR+MR1 group). AN was induced by tail vein injection of 5.2 mg/kg of adriamycin (ADR). Hamster IgG (control Ab) or MR1 was administered intraperitoneally on days 5, 7, 9 and 11 after ADR injection. Histological and functional data were collected 4 weeks after ADR injection. In vitro experiments tested the effect of soluble and cell-bound CD154 co-cultured with CD40-expressing cells [macrophages, mesangial cells and renal tubular epithelial cells (RTEC)]. Results. All experimental animals developed nephropathy. Compared to the ADR+IgG group, ADR+MR1 animals had significantly less histological injury (glomerulosclerosis and tubular atrophy) and functional injury (creatinine clearance). Kidneys of ADR+MR1 animals had significantly less macrophage infiltration than those of ADR+IgG animals. Interestingly, expression of CD40 and CD41 (a platelet-specific marker) was significantly less in ADR+MR1 animals compared to ADR+IgG animals. In vitro, CD154 blockade significantly attenuated upregulation of CCL2 gene expression by RTEC stimulated by activated macrophage-conditioned medium. In contrast, platelet-induced upregulation of macrophage and mesangial cell proinflammatory cytokine gene expression were not CD154-dependent. Conclusion. CD40–CD154 blockade has a significant innate renoprotective effect in ADR nephrosis. This is potentially due to inhibition of macrophage-derived soluble CD154.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfp569</identifier><identifier>PMID: 19889873</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Antibodies, Anti-Idiotypic - pharmacology ; Biological and medical sciences ; CD40 Antigens - antagonists & inhibitors ; CD40 Antigens - physiology ; CD40 Ligand - antagonists & inhibitors ; CD40 Ligand - physiology ; Chemokine CCL2 - physiology ; co-stimulation ; Cytokines - metabolism ; Disease Models, Animal ; Doxorubicin - adverse effects ; Emergency and intensive care: renal failure. Dialysis management ; Epithelial Cells - drug effects ; Epithelial Cells - immunology ; Epithelial Cells - pathology ; focal sclerosing glomerulonephritis ; Immunity, Innate - physiology ; Intensive care medicine ; Kidney Tubules - drug effects ; Kidney Tubules - immunology ; Kidney Tubules - pathology ; macrophages ; Macrophages - metabolism ; Macrophages - pathology ; Medical sciences ; Mesangial Cells - metabolism ; Mesangial Cells - pathology ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Nephrosis - chemically induced ; Nephrosis - pathology ; Nephrosis - physiopathology ; renal disease ; Signal Transduction - physiology ; tubulointerstitial injury ; Tubulopathies</subject><ispartof>Nephrology, dialysis, transplantation, 2010-03, Vol.25 (3), p.717-730</ispartof><rights>Oxford University Press © The Author 2009. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org 2009</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-7a17a66c5d1a102654d6e67e40697e74cb96663ac68357f2e6ddeb08d59a5c873</citedby><cites>FETCH-LOGICAL-c452t-7a17a66c5d1a102654d6e67e40697e74cb96663ac68357f2e6ddeb08d59a5c873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22680548$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19889873$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Vincent W.S.</creatorcontrib><creatorcontrib>Qin, Xiaohong</creatorcontrib><creatorcontrib>Wang, Yiping</creatorcontrib><creatorcontrib>Zheng, Guoping</creatorcontrib><creatorcontrib>Wang, Ya</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Ince, Jon</creatorcontrib><creatorcontrib>Tan, Thian K.</creatorcontrib><creatorcontrib>Kairaitis, Lukas K.</creatorcontrib><creatorcontrib>Alexander, Stephen I.</creatorcontrib><creatorcontrib>Harris, David C.H.</creatorcontrib><title>The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><addtitle>Nephrol Dial Transplant</addtitle><description>Background. Blockade of CD40–CD40 ligand (CD154) interactions protects against renal injury in adriamycin nephropathy (AN) in immunocompetent mice. To investigate whether this protection relied on adaptive or cognate immunity, we tested the effect of CD40–CD154 blockade in severe combined immunodeficient (SCID) mice. Methods. SCID mice were divided into three groups: normal, AN + hamster IgG (ADR+IgG group) and AN + anti-CD154 antibody (MR1) (ADR+MR1 group). AN was induced by tail vein injection of 5.2 mg/kg of adriamycin (ADR). Hamster IgG (control Ab) or MR1 was administered intraperitoneally on days 5, 7, 9 and 11 after ADR injection. Histological and functional data were collected 4 weeks after ADR injection. In vitro experiments tested the effect of soluble and cell-bound CD154 co-cultured with CD40-expressing cells [macrophages, mesangial cells and renal tubular epithelial cells (RTEC)]. Results. All experimental animals developed nephropathy. Compared to the ADR+IgG group, ADR+MR1 animals had significantly less histological injury (glomerulosclerosis and tubular atrophy) and functional injury (creatinine clearance). Kidneys of ADR+MR1 animals had significantly less macrophage infiltration than those of ADR+IgG animals. Interestingly, expression of CD40 and CD41 (a platelet-specific marker) was significantly less in ADR+MR1 animals compared to ADR+IgG animals. In vitro, CD154 blockade significantly attenuated upregulation of CCL2 gene expression by RTEC stimulated by activated macrophage-conditioned medium. In contrast, platelet-induced upregulation of macrophage and mesangial cell proinflammatory cytokine gene expression were not CD154-dependent. Conclusion. CD40–CD154 blockade has a significant innate renoprotective effect in ADR nephrosis. This is potentially due to inhibition of macrophage-derived soluble CD154.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Antibodies, Anti-Idiotypic - pharmacology</subject><subject>Biological and medical sciences</subject><subject>CD40 Antigens - antagonists & inhibitors</subject><subject>CD40 Antigens - physiology</subject><subject>CD40 Ligand - antagonists & inhibitors</subject><subject>CD40 Ligand - physiology</subject><subject>Chemokine CCL2 - physiology</subject><subject>co-stimulation</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Doxorubicin - adverse effects</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelial Cells - pathology</subject><subject>focal sclerosing glomerulonephritis</subject><subject>Immunity, Innate - physiology</subject><subject>Intensive care medicine</subject><subject>Kidney Tubules - drug effects</subject><subject>Kidney Tubules - immunology</subject><subject>Kidney Tubules - pathology</subject><subject>macrophages</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Medical sciences</subject><subject>Mesangial Cells - metabolism</subject><subject>Mesangial Cells - pathology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, SCID</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Nephrosis - chemically induced</subject><subject>Nephrosis - pathology</subject><subject>Nephrosis - physiopathology</subject><subject>renal disease</subject><subject>Signal Transduction - physiology</subject><subject>tubulointerstitial injury</subject><subject>Tubulopathies</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtKHEEUhgtJ0HHiJg8QehMCQmtdum7LMCZRMWShERGkOFNdnSnTXd2p6iaZXd4hb5gnscIMuour_8D5-A_nQ-g1wUcEa3Yc6vH4WzNwoXfQjFQCl5Qp_gLN8pKUmGO9h_ZTuscYayrlLtojWimtJJuhu6uVKxYnFf77-8_ihPCqsH2ZRt9NLYy-D8UA4-onrIvO1R5GlwofQs7Cd90UcoT7Ka5zFFBHD93a5jG4YRX75NMr9LKBNrmDbc7R148frhan5cWXT2eL9xelrTgdSwlEghCW1wQIpoJXtXBCugoLLZ2s7FILIRhYoRiXDXWirt0Sq5pr4Db_MUfvNr1D7H9MLo2m88m6toXg-ikZmaUoISh-nmSMMCqzuTk63JA2v5Kia8wQfQdxbQg2_7yb7N1svGf4zbZ2WmZTT-hWdAbebgFIFtomQrA-PXKUCoV5pZ64fhr-f7DccD6N7tcjCfG7EZJJbk5vbo3-zPWlvr415-wBxJqn0g</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Lee, Vincent W.S.</creator><creator>Qin, Xiaohong</creator><creator>Wang, Yiping</creator><creator>Zheng, Guoping</creator><creator>Wang, Ya</creator><creator>Wang, Ying</creator><creator>Ince, Jon</creator><creator>Tan, Thian K.</creator><creator>Kairaitis, Lukas K.</creator><creator>Alexander, Stephen I.</creator><creator>Harris, David C.H.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>IQODW</scope><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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20100301</creationdate><title>The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis</title><author>Lee, Vincent W.S. ; Qin, Xiaohong ; Wang, Yiping ; Zheng, Guoping ; Wang, Ya ; Wang, Ying ; Ince, Jon ; Tan, Thian K. ; Kairaitis, Lukas K. ; Alexander, Stephen I. ; Harris, David C.H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-7a17a66c5d1a102654d6e67e40697e74cb96663ac68357f2e6ddeb08d59a5c873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Antibodies, Anti-Idiotypic - pharmacology</topic><topic>Biological and medical sciences</topic><topic>CD40 Antigens - antagonists & inhibitors</topic><topic>CD40 Antigens - physiology</topic><topic>CD40 Ligand - antagonists & inhibitors</topic><topic>CD40 Ligand - physiology</topic><topic>Chemokine CCL2 - physiology</topic><topic>co-stimulation</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Doxorubicin - adverse effects</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - immunology</topic><topic>Epithelial Cells - pathology</topic><topic>focal sclerosing glomerulonephritis</topic><topic>Immunity, Innate - physiology</topic><topic>Intensive care medicine</topic><topic>Kidney Tubules - drug effects</topic><topic>Kidney Tubules - immunology</topic><topic>Kidney Tubules - pathology</topic><topic>macrophages</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Medical sciences</topic><topic>Mesangial Cells - metabolism</topic><topic>Mesangial Cells - pathology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, SCID</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Nephrosis - chemically induced</topic><topic>Nephrosis - pathology</topic><topic>Nephrosis - physiopathology</topic><topic>renal disease</topic><topic>Signal Transduction - physiology</topic><topic>tubulointerstitial injury</topic><topic>Tubulopathies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Vincent W.S.</creatorcontrib><creatorcontrib>Qin, Xiaohong</creatorcontrib><creatorcontrib>Wang, Yiping</creatorcontrib><creatorcontrib>Zheng, Guoping</creatorcontrib><creatorcontrib>Wang, Ya</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Ince, Jon</creatorcontrib><creatorcontrib>Tan, Thian K.</creatorcontrib><creatorcontrib>Kairaitis, Lukas K.</creatorcontrib><creatorcontrib>Alexander, Stephen I.</creatorcontrib><creatorcontrib>Harris, David C.H.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Vincent W.S.</au><au>Qin, Xiaohong</au><au>Wang, Yiping</au><au>Zheng, Guoping</au><au>Wang, Ya</au><au>Wang, Ying</au><au>Ince, Jon</au><au>Tan, Thian K.</au><au>Kairaitis, Lukas K.</au><au>Alexander, Stephen I.</au><au>Harris, David C.H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><stitle>Nephrol Dial Transplant</stitle><addtitle>Nephrol Dial Transplant</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>25</volume><issue>3</issue><spage>717</spage><epage>730</epage><pages>717-730</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Blockade of CD40–CD40 ligand (CD154) interactions protects against renal injury in adriamycin nephropathy (AN) in immunocompetent mice. To investigate whether this protection relied on adaptive or cognate immunity, we tested the effect of CD40–CD154 blockade in severe combined immunodeficient (SCID) mice. Methods. SCID mice were divided into three groups: normal, AN + hamster IgG (ADR+IgG group) and AN + anti-CD154 antibody (MR1) (ADR+MR1 group). AN was induced by tail vein injection of 5.2 mg/kg of adriamycin (ADR). Hamster IgG (control Ab) or MR1 was administered intraperitoneally on days 5, 7, 9 and 11 after ADR injection. Histological and functional data were collected 4 weeks after ADR injection. In vitro experiments tested the effect of soluble and cell-bound CD154 co-cultured with CD40-expressing cells [macrophages, mesangial cells and renal tubular epithelial cells (RTEC)]. Results. All experimental animals developed nephropathy. Compared to the ADR+IgG group, ADR+MR1 animals had significantly less histological injury (glomerulosclerosis and tubular atrophy) and functional injury (creatinine clearance). Kidneys of ADR+MR1 animals had significantly less macrophage infiltration than those of ADR+IgG animals. Interestingly, expression of CD40 and CD41 (a platelet-specific marker) was significantly less in ADR+MR1 animals compared to ADR+IgG animals. In vitro, CD154 blockade significantly attenuated upregulation of CCL2 gene expression by RTEC stimulated by activated macrophage-conditioned medium. In contrast, platelet-induced upregulation of macrophage and mesangial cell proinflammatory cytokine gene expression were not CD154-dependent. Conclusion. CD40–CD154 blockade has a significant innate renoprotective effect in ADR nephrosis. This is potentially due to inhibition of macrophage-derived soluble CD154.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>19889873</pmid><doi>10.1093/ndt/gfp569</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0931-0509 |
| ispartof | Nephrology, dialysis, transplantation, 2010-03, Vol.25 (3), p.717-730 |
| issn | 0931-0509 1460-2385 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_746086620 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Antibodies, Anti-Idiotypic - pharmacology Biological and medical sciences CD40 Antigens - antagonists & inhibitors CD40 Antigens - physiology CD40 Ligand - antagonists & inhibitors CD40 Ligand - physiology Chemokine CCL2 - physiology co-stimulation Cytokines - metabolism Disease Models, Animal Doxorubicin - adverse effects Emergency and intensive care: renal failure. Dialysis management Epithelial Cells - drug effects Epithelial Cells - immunology Epithelial Cells - pathology focal sclerosing glomerulonephritis Immunity, Innate - physiology Intensive care medicine Kidney Tubules - drug effects Kidney Tubules - immunology Kidney Tubules - pathology macrophages Macrophages - metabolism Macrophages - pathology Medical sciences Mesangial Cells - metabolism Mesangial Cells - pathology Mice Mice, Inbred BALB C Mice, SCID Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Nephrosis - chemically induced Nephrosis - pathology Nephrosis - physiopathology renal disease Signal Transduction - physiology tubulointerstitial injury Tubulopathies |
| title | The CD40–CD154 co-stimulation pathway mediates innate immune injury in adriamycin nephrosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T20%3A37%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20CD40%E2%80%93CD154%20co-stimulation%20pathway%20mediates%20innate%20immune%20injury%20in%20adriamycin%20nephrosis&rft.jtitle=Nephrology,%20dialysis,%20transplantation&rft.au=Lee,%20Vincent%20W.S.&rft.date=2010-03-01&rft.volume=25&rft.issue=3&rft.spage=717&rft.epage=730&rft.pages=717-730&rft.issn=0931-0509&rft.eissn=1460-2385&rft.coden=NDTREA&rft_id=info:doi/10.1093/ndt/gfp569&rft_dat=%3Cproquest_cross%3E746086620%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=733132709&rft_id=info:pmid/19889873&rft_oup_id=10.1093/ndt/gfp569&rfr_iscdi=true |