Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease
Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease. Interaction between CD40 and CD40 ligand (CD40L) is involved in both cognate and innate immune responses. Blockade of CD40-CD40L interactions reduces severity of renal injury in murine lupus nephritis an...
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| description | Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease.
Interaction between CD40 and CD40 ligand (CD40L) is involved in both cognate and innate immune responses. Blockade of CD40-CD40L interactions reduces severity of renal injury in murine lupus nephritis and membranous nephropathy. We hypothesized that CD40-CD40L could contribute to renal injury in models that are not antibody-dependent, and that anti-CD40L could diminish inflammation and fibrosis in murine adriamycin nephropathy.
Male BALB/c mice were divided into three groups (N = 6 per group): (1) saline-treated, age-matched control; (2) adriamycin only; and (3) MR1 + adriamycin. In group 3, mice were treated with intraperitoneal injections of anti-CD40L antibody (clone MR1, 0.4mg per mouse) after the onset of proteinuria at days 5, 7, 9, and 11 after adriamycin treatment. Animal subgroups were compared at 14 and 42 days after induction of adriamycin nephropathy. Functional and pathologic markers of disease severity, cellular components of interstitial inflammation, and the degree of CD40 expression were assessed. Relative cortical RNA expression of the chemokine monocyte-chemoattractant protein-1 (MCP-1) and regulated on activation normal T cell expressed and secreted (RANTES) was also compared between animal groups.
CD40 was weakly expressed in tubules of normal mice but was expressed in tubules, interstitium, and glomeruli of mice with adriamycin nephropathy in a time-dependent manner. MR1 treatment resulted in a significant attenuation of the severity of adriamycin nephropathy at day 42 [e.g., glomerular sclerosis (%), group 3, 20.1 ± 4.7 vs. group 2, 30.2 ± 7.2, P < 0.001]. CD40L blockade significantly reduced tubulointerstitial injury as well [tubular diameter (μm), group 3, 42.5 ± 6.9 vs. group 2, 66.3 ± 13.7, P < 0.001; and group 1, 37.3 ± 5.7, P < 0.01; tubular cell height (μm), group 3, 16.3 ± 1.7 vs. group 2, 11 ± 1.8, P < 0.01; and group 1, 18.2 ± 1.9, P < 0.01; interstitial volume (%), group 3, 13.9 ± 5.1 vs. group 2, 26.2 ± 4.9, P < 0.001; and group 1, 1.3 ± 0.7, P < 0.001; proteinuria (mg/24 hours), group 3, 1.8 ± 0.6 vs. group 2, 4.3 ± 0.8, P < 0.001; and group 1, 0.7 ± 0.2, P < 0.05; and creatinine clearance (μL/min), group 3, 75 ± 4 vs. group 2, 35 ± 2, P < 0.001; and group 1, 82 ± 4, P < 0.01] were also improved by MR1. MR1 treatment also resulted in a significant reduction in the number of cortical macrophages at both 14 and 42 days after ad |
| doi_str_mv | 10.1046/j.1523-1755.2003.00223.x |
| format | Article |
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Interaction between CD40 and CD40 ligand (CD40L) is involved in both cognate and innate immune responses. Blockade of CD40-CD40L interactions reduces severity of renal injury in murine lupus nephritis and membranous nephropathy. We hypothesized that CD40-CD40L could contribute to renal injury in models that are not antibody-dependent, and that anti-CD40L could diminish inflammation and fibrosis in murine adriamycin nephropathy.
Male BALB/c mice were divided into three groups (N = 6 per group): (1) saline-treated, age-matched control; (2) adriamycin only; and (3) MR1 + adriamycin. In group 3, mice were treated with intraperitoneal injections of anti-CD40L antibody (clone MR1, 0.4mg per mouse) after the onset of proteinuria at days 5, 7, 9, and 11 after adriamycin treatment. Animal subgroups were compared at 14 and 42 days after induction of adriamycin nephropathy. Functional and pathologic markers of disease severity, cellular components of interstitial inflammation, and the degree of CD40 expression were assessed. Relative cortical RNA expression of the chemokine monocyte-chemoattractant protein-1 (MCP-1) and regulated on activation normal T cell expressed and secreted (RANTES) was also compared between animal groups.
CD40 was weakly expressed in tubules of normal mice but was expressed in tubules, interstitium, and glomeruli of mice with adriamycin nephropathy in a time-dependent manner. MR1 treatment resulted in a significant attenuation of the severity of adriamycin nephropathy at day 42 [e.g., glomerular sclerosis (%), group 3, 20.1 ± 4.7 vs. group 2, 30.2 ± 7.2, P < 0.001]. CD40L blockade significantly reduced tubulointerstitial injury as well [tubular diameter (μm), group 3, 42.5 ± 6.9 vs. group 2, 66.3 ± 13.7, P < 0.001; and group 1, 37.3 ± 5.7, P < 0.01; tubular cell height (μm), group 3, 16.3 ± 1.7 vs. group 2, 11 ± 1.8, P < 0.01; and group 1, 18.2 ± 1.9, P < 0.01; interstitial volume (%), group 3, 13.9 ± 5.1 vs. group 2, 26.2 ± 4.9, P < 0.001; and group 1, 1.3 ± 0.7, P < 0.001; proteinuria (mg/24 hours), group 3, 1.8 ± 0.6 vs. group 2, 4.3 ± 0.8, P < 0.001; and group 1, 0.7 ± 0.2, P < 0.05; and creatinine clearance (μL/min), group 3, 75 ± 4 vs. group 2, 35 ± 2, P < 0.001; and group 1, 82 ± 4, P < 0.01] were also improved by MR1. MR1 treatment also resulted in a significant reduction in the number of cortical macrophages at both 14 and 42 days after adriamycin (P < 0.01). Cortical expression of MCP-1 and RANTES was significantly reduced by MR1 treatment at 42 days after adriamycin (P < 0.01 and P < 0.05, respectively).
Blockade of CD40-CD40L interaction protects against renal structural and functional injury in this murine model of chronic proteinuric renal disease.]]></description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2003.00223.x</identifier><identifier>PMID: 12969144</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>adriamycin nephrosis ; Animals ; Antibodies - pharmacology ; Biological and medical sciences ; blockade ; CD40 Antigens - immunology ; CD40 Antigens - metabolism ; CD40 ligand ; CD40 Ligand - immunology ; Chemokine CCL2 - metabolism ; Chemokine CCL5 - metabolism ; Chronic Disease ; Doxorubicin ; Kidney - drug effects ; Kidney - pathology ; Kidney - physiopathology ; Kidney Cortex - metabolism ; Kidneys ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Monocytes - pathology ; Nephrology. Urinary tract diseases ; Nephrosis - chemically induced ; Nephrosis - pathology ; Nephrosis - physiopathology ; Proteinuria - drug therapy ; Urinary system involvement in other diseases. Miscellaneous</subject><ispartof>Kidney international, 2003-10, Vol.64 (4), p.1265-1272</ispartof><rights>2003 International Society of Nephrology</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Oct 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c597t-7a077f65bfdc4c3778930fd1b1f531bd0d11ec7b74d121d1c6e236ad5c2e0ee33</citedby><cites>FETCH-LOGICAL-c597t-7a077f65bfdc4c3778930fd1b1f531bd0d11ec7b74d121d1c6e236ad5c2e0ee33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210102183?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15140825$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12969144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kairaitis, Lukas</creatorcontrib><creatorcontrib>Wang, Yiping</creatorcontrib><creatorcontrib>Zheng, Ling</creatorcontrib><creatorcontrib>Tay, Yuet-Ching</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Harris, David C.H.</creatorcontrib><title>Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description><![CDATA[Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease.
Interaction between CD40 and CD40 ligand (CD40L) is involved in both cognate and innate immune responses. Blockade of CD40-CD40L interactions reduces severity of renal injury in murine lupus nephritis and membranous nephropathy. We hypothesized that CD40-CD40L could contribute to renal injury in models that are not antibody-dependent, and that anti-CD40L could diminish inflammation and fibrosis in murine adriamycin nephropathy.
Male BALB/c mice were divided into three groups (N = 6 per group): (1) saline-treated, age-matched control; (2) adriamycin only; and (3) MR1 + adriamycin. In group 3, mice were treated with intraperitoneal injections of anti-CD40L antibody (clone MR1, 0.4mg per mouse) after the onset of proteinuria at days 5, 7, 9, and 11 after adriamycin treatment. Animal subgroups were compared at 14 and 42 days after induction of adriamycin nephropathy. Functional and pathologic markers of disease severity, cellular components of interstitial inflammation, and the degree of CD40 expression were assessed. Relative cortical RNA expression of the chemokine monocyte-chemoattractant protein-1 (MCP-1) and regulated on activation normal T cell expressed and secreted (RANTES) was also compared between animal groups.
CD40 was weakly expressed in tubules of normal mice but was expressed in tubules, interstitium, and glomeruli of mice with adriamycin nephropathy in a time-dependent manner. MR1 treatment resulted in a significant attenuation of the severity of adriamycin nephropathy at day 42 [e.g., glomerular sclerosis (%), group 3, 20.1 ± 4.7 vs. group 2, 30.2 ± 7.2, P < 0.001]. CD40L blockade significantly reduced tubulointerstitial injury as well [tubular diameter (μm), group 3, 42.5 ± 6.9 vs. group 2, 66.3 ± 13.7, P < 0.001; and group 1, 37.3 ± 5.7, P < 0.01; tubular cell height (μm), group 3, 16.3 ± 1.7 vs. group 2, 11 ± 1.8, P < 0.01; and group 1, 18.2 ± 1.9, P < 0.01; interstitial volume (%), group 3, 13.9 ± 5.1 vs. group 2, 26.2 ± 4.9, P < 0.001; and group 1, 1.3 ± 0.7, P < 0.001; proteinuria (mg/24 hours), group 3, 1.8 ± 0.6 vs. group 2, 4.3 ± 0.8, P < 0.001; and group 1, 0.7 ± 0.2, P < 0.05; and creatinine clearance (μL/min), group 3, 75 ± 4 vs. group 2, 35 ± 2, P < 0.001; and group 1, 82 ± 4, P < 0.01] were also improved by MR1. MR1 treatment also resulted in a significant reduction in the number of cortical macrophages at both 14 and 42 days after adriamycin (P < 0.01). Cortical expression of MCP-1 and RANTES was significantly reduced by MR1 treatment at 42 days after adriamycin (P < 0.01 and P < 0.05, respectively).
Blockade of CD40-CD40L interaction protects against renal structural and functional injury in this murine model of chronic proteinuric renal disease.]]></description><subject>adriamycin nephrosis</subject><subject>Animals</subject><subject>Antibodies - pharmacology</subject><subject>Biological and medical sciences</subject><subject>blockade</subject><subject>CD40 Antigens - immunology</subject><subject>CD40 Antigens - metabolism</subject><subject>CD40 ligand</subject><subject>CD40 Ligand - immunology</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokine CCL5 - metabolism</subject><subject>Chronic Disease</subject><subject>Doxorubicin</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney Cortex - metabolism</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Monocytes - pathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephrosis - chemically induced</subject><subject>Nephrosis - pathology</subject><subject>Nephrosis - physiopathology</subject><subject>Proteinuria - drug therapy</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkUtv1TAQhS0EorcXfgLIQkKsEjx-5LGkFwpIldjA2nLsSXHIdYqdVO2_xyFXrcSGjcej-WZ0dA4hFFgJTFbvhxIUFwXUSpWcMVEyxrko756Q3cPgKdkx1qiCK9GckfOUBpb7VrDn5Ax4W7Ug5Y7oi3Gyv4xDOvX08FGyYn3o6K9NcPQmTjPaOVFzbXxIM40YzEh9GJZ4nwu1P-MUvN1AH5aY_xvjfEKT8AV51psx4ctT3ZMfl5--H74UV98-fz18uCqsauu5qA2r675SXe-stKKuV6G9gw56JaBzzAGgrbtaOuDgwFbIRWWcshwZohB78m67m5X8XjDN-uiTxXE0Aacl6WwICAGqzeSbf8hhWmKWnDQHBoxDs55rNsjGKaWIvb6J_mjivQam1wj0oFen9eq0XiPQfyPQd3n19en-0h3RPS6ePM_A2xNgkjVjH02wPj1yCiRrcmp78mrjgpmXiA-AlK1kWeSeXGxzzL7eeow6WY_BovMxh6bd5P-v9g_1za1X</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Kairaitis, Lukas</creator><creator>Wang, Yiping</creator><creator>Zheng, Ling</creator><creator>Tay, Yuet-Ching</creator><creator>Wang, Yang</creator><creator>Harris, David C.H.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20031001</creationdate><title>Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease</title><author>Kairaitis, Lukas ; Wang, Yiping ; Zheng, Ling ; Tay, Yuet-Ching ; Wang, Yang ; Harris, David C.H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c597t-7a077f65bfdc4c3778930fd1b1f531bd0d11ec7b74d121d1c6e236ad5c2e0ee33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>adriamycin nephrosis</topic><topic>Animals</topic><topic>Antibodies - pharmacology</topic><topic>Biological and medical sciences</topic><topic>blockade</topic><topic>CD40 Antigens - immunology</topic><topic>CD40 Antigens - metabolism</topic><topic>CD40 ligand</topic><topic>CD40 Ligand - immunology</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokine CCL5 - metabolism</topic><topic>Chronic Disease</topic><topic>Doxorubicin</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney Cortex - metabolism</topic><topic>Kidneys</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Monocytes - pathology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephrosis - chemically induced</topic><topic>Nephrosis - pathology</topic><topic>Nephrosis - physiopathology</topic><topic>Proteinuria - drug therapy</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kairaitis, Lukas</creatorcontrib><creatorcontrib>Wang, Yiping</creatorcontrib><creatorcontrib>Zheng, Ling</creatorcontrib><creatorcontrib>Tay, Yuet-Ching</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Harris, David C.H.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kairaitis, Lukas</au><au>Wang, Yiping</au><au>Zheng, Ling</au><au>Tay, Yuet-Ching</au><au>Wang, Yang</au><au>Harris, David C.H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>64</volume><issue>4</issue><spage>1265</spage><epage>1272</epage><pages>1265-1272</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract><![CDATA[Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease.
Interaction between CD40 and CD40 ligand (CD40L) is involved in both cognate and innate immune responses. Blockade of CD40-CD40L interactions reduces severity of renal injury in murine lupus nephritis and membranous nephropathy. We hypothesized that CD40-CD40L could contribute to renal injury in models that are not antibody-dependent, and that anti-CD40L could diminish inflammation and fibrosis in murine adriamycin nephropathy.
Male BALB/c mice were divided into three groups (N = 6 per group): (1) saline-treated, age-matched control; (2) adriamycin only; and (3) MR1 + adriamycin. In group 3, mice were treated with intraperitoneal injections of anti-CD40L antibody (clone MR1, 0.4mg per mouse) after the onset of proteinuria at days 5, 7, 9, and 11 after adriamycin treatment. Animal subgroups were compared at 14 and 42 days after induction of adriamycin nephropathy. Functional and pathologic markers of disease severity, cellular components of interstitial inflammation, and the degree of CD40 expression were assessed. Relative cortical RNA expression of the chemokine monocyte-chemoattractant protein-1 (MCP-1) and regulated on activation normal T cell expressed and secreted (RANTES) was also compared between animal groups.
CD40 was weakly expressed in tubules of normal mice but was expressed in tubules, interstitium, and glomeruli of mice with adriamycin nephropathy in a time-dependent manner. MR1 treatment resulted in a significant attenuation of the severity of adriamycin nephropathy at day 42 [e.g., glomerular sclerosis (%), group 3, 20.1 ± 4.7 vs. group 2, 30.2 ± 7.2, P < 0.001]. CD40L blockade significantly reduced tubulointerstitial injury as well [tubular diameter (μm), group 3, 42.5 ± 6.9 vs. group 2, 66.3 ± 13.7, P < 0.001; and group 1, 37.3 ± 5.7, P < 0.01; tubular cell height (μm), group 3, 16.3 ± 1.7 vs. group 2, 11 ± 1.8, P < 0.01; and group 1, 18.2 ± 1.9, P < 0.01; interstitial volume (%), group 3, 13.9 ± 5.1 vs. group 2, 26.2 ± 4.9, P < 0.001; and group 1, 1.3 ± 0.7, P < 0.001; proteinuria (mg/24 hours), group 3, 1.8 ± 0.6 vs. group 2, 4.3 ± 0.8, P < 0.001; and group 1, 0.7 ± 0.2, P < 0.05; and creatinine clearance (μL/min), group 3, 75 ± 4 vs. group 2, 35 ± 2, P < 0.001; and group 1, 82 ± 4, P < 0.01] were also improved by MR1. MR1 treatment also resulted in a significant reduction in the number of cortical macrophages at both 14 and 42 days after adriamycin (P < 0.01). Cortical expression of MCP-1 and RANTES was significantly reduced by MR1 treatment at 42 days after adriamycin (P < 0.01 and P < 0.05, respectively).
Blockade of CD40-CD40L interaction protects against renal structural and functional injury in this murine model of chronic proteinuric renal disease.]]></abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12969144</pmid><doi>10.1046/j.1523-1755.2003.00223.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 2003-10, Vol.64 (4), p.1265-1272 |
| issn | 0085-2538 1523-1755 |
| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
| subjects | adriamycin nephrosis Animals Antibodies - pharmacology Biological and medical sciences blockade CD40 Antigens - immunology CD40 Antigens - metabolism CD40 ligand CD40 Ligand - immunology Chemokine CCL2 - metabolism Chemokine CCL5 - metabolism Chronic Disease Doxorubicin Kidney - drug effects Kidney - pathology Kidney - physiopathology Kidney Cortex - metabolism Kidneys Male Medical sciences Mice Mice, Inbred BALB C Monocytes - pathology Nephrology. Urinary tract diseases Nephrosis - chemically induced Nephrosis - pathology Nephrosis - physiopathology Proteinuria - drug therapy Urinary system involvement in other diseases. Miscellaneous |
| title | Blockade of CD40-CD40 ligand protects against renal injury in chronic proteinuric renal disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T17%3A30%3A56IST&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=Blockade%20of%20CD40-CD40%20ligand%20protects%20against%20renal%20injury%20in%20chronic%20proteinuric%20renal%20disease&rft.jtitle=Kidney%20international&rft.au=Kairaitis,%20Lukas&rft.date=2003-10-01&rft.volume=64&rft.issue=4&rft.spage=1265&rft.epage=1272&rft.pages=1265-1272&rft.issn=0085-2538&rft.eissn=1523-1755&rft.coden=KDYIA5&rft_id=info:doi/10.1046/j.1523-1755.2003.00223.x&rft_dat=%3Cproquest_cross%3E1012074671%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=210102183&rft_id=info:pmid/12969144&rft_els_id=S0085253815494621&rfr_iscdi=true |