Strain susceptibility to active induction and passive transfer of experimental autoimmune glomerulonephritis in the rat
Background. Previous studies have shown that different inbred rat strains vary in their susceptibility to experimental autoimmune glomerulonephritis (EAG). The Wistar Kyoto (WKY) rat is highly susceptible and develops crescentic glomerulonephritis, while the Lewis (LEW) rat is resistant. When immuni...
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| creator | Reynolds, John Albouainain, Amina Duda, Mark Anthony Evans, David John Pusey, Charles Dickson |
| description | Background. Previous studies have shown that different inbred rat strains vary in their susceptibility to experimental autoimmune glomerulonephritis (EAG). The Wistar Kyoto (WKY) rat is highly susceptible and develops crescentic glomerulonephritis, while the Lewis (LEW) rat is resistant. When immunized with collagenase-solubilized rat glomerular basement membrane (GBM), both strains produce circulating autoantibodies reactive with rat GBM by enzyme-linked immunosorbent assay, but only the WKY rat shows strong linear deposits of IgG on the GBM. Methods. We investigated the hypothesis that differences in the characteristics of the anti-GBM antibodies produced, or in the inflammatory response to antibody deposition, could account for susceptibility. Results. We found that circulating anti-GBM antibodies from WKY rats immunized with GBM were present at a higher concentration than those from LEW rats. Antibodies from WKY rats also recognized the rat α3 chain of type IV collagen [α3(IV)NC1], whereas those from LEW rats did not. Antibody eluted from the kidneys of WKY rats with EAG induced by GBM showed a higher affinity for GBM and recombinant rat α3(IV)NC1 than circulating antibody. This eluted antibody bound strongly to normal kidney sections from both WKY and LEW rats. Passive transfer of eluted anti-GBM antibodies from WKY rats with EAG resulted in similar binding of IgG to the GBM of WKY and LEW rats at 24 h. However, only the WKY recipients went on to develop crescentic glomerulonephritis by 28 days. Conclusions. This study demonstrates that the characteristics of the anti-GBM antibodies induced in WKY rats contribute to their susceptibility to EAG. However, the passive transfer experiments reveal that factors related to the inflammatory response to antibody deposition are also important in determining susceptibility. A combination of these genetic influences could explain the variation in severity of human anti-GBM disease. |
| doi_str_mv | 10.1093/ndt/gfl523 |
| format | Article |
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Previous studies have shown that different inbred rat strains vary in their susceptibility to experimental autoimmune glomerulonephritis (EAG). The Wistar Kyoto (WKY) rat is highly susceptible and develops crescentic glomerulonephritis, while the Lewis (LEW) rat is resistant. When immunized with collagenase-solubilized rat glomerular basement membrane (GBM), both strains produce circulating autoantibodies reactive with rat GBM by enzyme-linked immunosorbent assay, but only the WKY rat shows strong linear deposits of IgG on the GBM. Methods. We investigated the hypothesis that differences in the characteristics of the anti-GBM antibodies produced, or in the inflammatory response to antibody deposition, could account for susceptibility. Results. We found that circulating anti-GBM antibodies from WKY rats immunized with GBM were present at a higher concentration than those from LEW rats. Antibodies from WKY rats also recognized the rat α3 chain of type IV collagen [α3(IV)NC1], whereas those from LEW rats did not. Antibody eluted from the kidneys of WKY rats with EAG induced by GBM showed a higher affinity for GBM and recombinant rat α3(IV)NC1 than circulating antibody. This eluted antibody bound strongly to normal kidney sections from both WKY and LEW rats. Passive transfer of eluted anti-GBM antibodies from WKY rats with EAG resulted in similar binding of IgG to the GBM of WKY and LEW rats at 24 h. However, only the WKY recipients went on to develop crescentic glomerulonephritis by 28 days. Conclusions. This study demonstrates that the characteristics of the anti-GBM antibodies induced in WKY rats contribute to their susceptibility to EAG. However, the passive transfer experiments reveal that factors related to the inflammatory response to antibody deposition are also important in determining susceptibility. A combination of these genetic influences could explain the variation in severity of human anti-GBM disease.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfl523</identifier><identifier>PMID: 16998225</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 ; anti-GBM antibodies ; Autoimmune Diseases - genetics ; Biological and medical sciences ; Emergency and intensive care: renal failure. Dialysis management ; experimental autoimmune glomerulonephritis (EAG) ; Genetic Predisposition to Disease ; genetic susceptibility ; glomerular basement membrane (GBM) ; Glomerulonephritis ; Glomerulonephritis - genetics ; Glomerulonephritis - immunology ; Human viral diseases ; Infectious diseases ; Intensive care medicine ; Lewis (LEW) rat ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Rats ; Rats, Inbred Lew ; Rats, Inbred WKY ; Viral diseases ; Viral hepatitis ; Wistar Kyoto (WKY) rat</subject><ispartof>Nephrology, dialysis, transplantation, 2006-12, Vol.21 (12), p.3398-3408</ispartof><rights>2007 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Dec 1, 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-37879fdac78ffd39afdc24ee60078f02daad6616d540d103948948f52f70e56d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18385225$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16998225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reynolds, John</creatorcontrib><creatorcontrib>Albouainain, Amina</creatorcontrib><creatorcontrib>Duda, Mark Anthony</creatorcontrib><creatorcontrib>Evans, David John</creatorcontrib><creatorcontrib>Pusey, Charles Dickson</creatorcontrib><title>Strain susceptibility to active induction and passive transfer of experimental autoimmune glomerulonephritis in the rat</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><description>Background. Previous studies have shown that different inbred rat strains vary in their susceptibility to experimental autoimmune glomerulonephritis (EAG). The Wistar Kyoto (WKY) rat is highly susceptible and develops crescentic glomerulonephritis, while the Lewis (LEW) rat is resistant. When immunized with collagenase-solubilized rat glomerular basement membrane (GBM), both strains produce circulating autoantibodies reactive with rat GBM by enzyme-linked immunosorbent assay, but only the WKY rat shows strong linear deposits of IgG on the GBM. Methods. We investigated the hypothesis that differences in the characteristics of the anti-GBM antibodies produced, or in the inflammatory response to antibody deposition, could account for susceptibility. Results. We found that circulating anti-GBM antibodies from WKY rats immunized with GBM were present at a higher concentration than those from LEW rats. Antibodies from WKY rats also recognized the rat α3 chain of type IV collagen [α3(IV)NC1], whereas those from LEW rats did not. Antibody eluted from the kidneys of WKY rats with EAG induced by GBM showed a higher affinity for GBM and recombinant rat α3(IV)NC1 than circulating antibody. This eluted antibody bound strongly to normal kidney sections from both WKY and LEW rats. Passive transfer of eluted anti-GBM antibodies from WKY rats with EAG resulted in similar binding of IgG to the GBM of WKY and LEW rats at 24 h. However, only the WKY recipients went on to develop crescentic glomerulonephritis by 28 days. Conclusions. This study demonstrates that the characteristics of the anti-GBM antibodies induced in WKY rats contribute to their susceptibility to EAG. However, the passive transfer experiments reveal that factors related to the inflammatory response to antibody deposition are also important in determining susceptibility. A combination of these genetic influences could explain the variation in severity of human anti-GBM disease.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>anti-GBM antibodies</subject><subject>Autoimmune Diseases - genetics</subject><subject>Biological and medical sciences</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>experimental autoimmune glomerulonephritis (EAG)</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic susceptibility</subject><subject>glomerular basement membrane (GBM)</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis - genetics</subject><subject>Glomerulonephritis - immunology</subject><subject>Human viral diseases</subject><subject>Infectious diseases</subject><subject>Intensive care medicine</subject><subject>Lewis (LEW) rat</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Rats, Inbred WKY</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><subject>Wistar Kyoto (WKY) rat</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1rFTEQhoNY7OnRG3-ABMFeCGvzcZLdXJZDa9WC4BfiTUg3kzZ1N1mTrG3_vSl7sOCNMGTCzDMvzLwIPafkDSWKHwVbji7dIBh_hFZ0I0nDeCceo1Vt0oYIovbRQc7XhBDF2vYJ2qdSqY4xsUI3n0syPuA85x6m4i_84MsdLhGbvvjfgH2wc_3FgE2weDI531frUMgOEo4Ow-0EyY8QihmwmUv04zgHwJdDHCHNQwwwXSVffK5iuFwBTqY8RXvODBme7fIafT09-bI9a84_vn23PT5vekF5aXjbtcpZ07edc5Yr42zPNgCSkFohzBpjpaTSig2xlHC16Wo4wVxLQEjL1-hw0Z1S_DVDLnr0ddNhMAHinLXsqCCiZf8FqeJKsPqu0ct_wOs4p1CX0IxWNUl5V6HXC9SnmHMCp6d6IpPuNCX63jRdTdOLaRV-sVOcL0awD-jOpQq82gEm92Zw9fi9zw9cV-1euGbhfC5w-7dv0k8tW94Kffb9h95--sY_kPdEM_4HNf-xsw</recordid><startdate>20061201</startdate><enddate>20061201</enddate><creator>Reynolds, John</creator><creator>Albouainain, Amina</creator><creator>Duda, Mark Anthony</creator><creator>Evans, David John</creator><creator>Pusey, Charles Dickson</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</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>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20061201</creationdate><title>Strain susceptibility to active induction and passive transfer of experimental autoimmune glomerulonephritis in the rat</title><author>Reynolds, John ; Albouainain, Amina ; Duda, Mark Anthony ; Evans, David John ; Pusey, Charles Dickson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-37879fdac78ffd39afdc24ee60078f02daad6616d540d103948948f52f70e56d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>anti-GBM antibodies</topic><topic>Autoimmune Diseases - genetics</topic><topic>Biological and medical sciences</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>experimental autoimmune glomerulonephritis (EAG)</topic><topic>Genetic Predisposition to Disease</topic><topic>genetic susceptibility</topic><topic>glomerular basement membrane (GBM)</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis - genetics</topic><topic>Glomerulonephritis - immunology</topic><topic>Human viral diseases</topic><topic>Infectious diseases</topic><topic>Intensive care medicine</topic><topic>Lewis (LEW) rat</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Rats, Inbred WKY</topic><topic>Viral diseases</topic><topic>Viral hepatitis</topic><topic>Wistar Kyoto (WKY) rat</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reynolds, John</creatorcontrib><creatorcontrib>Albouainain, Amina</creatorcontrib><creatorcontrib>Duda, Mark Anthony</creatorcontrib><creatorcontrib>Evans, David John</creatorcontrib><creatorcontrib>Pusey, Charles Dickson</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reynolds, John</au><au>Albouainain, Amina</au><au>Duda, Mark Anthony</au><au>Evans, David John</au><au>Pusey, Charles Dickson</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Strain susceptibility to active induction and passive transfer of experimental autoimmune glomerulonephritis in the rat</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><addtitle>Nephrol Dial Transplant</addtitle><date>2006-12-01</date><risdate>2006</risdate><volume>21</volume><issue>12</issue><spage>3398</spage><epage>3408</epage><pages>3398-3408</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Previous studies have shown that different inbred rat strains vary in their susceptibility to experimental autoimmune glomerulonephritis (EAG). The Wistar Kyoto (WKY) rat is highly susceptible and develops crescentic glomerulonephritis, while the Lewis (LEW) rat is resistant. When immunized with collagenase-solubilized rat glomerular basement membrane (GBM), both strains produce circulating autoantibodies reactive with rat GBM by enzyme-linked immunosorbent assay, but only the WKY rat shows strong linear deposits of IgG on the GBM. Methods. We investigated the hypothesis that differences in the characteristics of the anti-GBM antibodies produced, or in the inflammatory response to antibody deposition, could account for susceptibility. Results. We found that circulating anti-GBM antibodies from WKY rats immunized with GBM were present at a higher concentration than those from LEW rats. Antibodies from WKY rats also recognized the rat α3 chain of type IV collagen [α3(IV)NC1], whereas those from LEW rats did not. Antibody eluted from the kidneys of WKY rats with EAG induced by GBM showed a higher affinity for GBM and recombinant rat α3(IV)NC1 than circulating antibody. This eluted antibody bound strongly to normal kidney sections from both WKY and LEW rats. Passive transfer of eluted anti-GBM antibodies from WKY rats with EAG resulted in similar binding of IgG to the GBM of WKY and LEW rats at 24 h. However, only the WKY recipients went on to develop crescentic glomerulonephritis by 28 days. Conclusions. This study demonstrates that the characteristics of the anti-GBM antibodies induced in WKY rats contribute to their susceptibility to EAG. However, the passive transfer experiments reveal that factors related to the inflammatory response to antibody deposition are also important in determining susceptibility. A combination of these genetic influences could explain the variation in severity of human anti-GBM disease.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>16998225</pmid><doi>10.1093/ndt/gfl523</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals anti-GBM antibodies Autoimmune Diseases - genetics Biological and medical sciences Emergency and intensive care: renal failure. Dialysis management experimental autoimmune glomerulonephritis (EAG) Genetic Predisposition to Disease genetic susceptibility glomerular basement membrane (GBM) Glomerulonephritis Glomerulonephritis - genetics Glomerulonephritis - immunology Human viral diseases Infectious diseases Intensive care medicine Lewis (LEW) rat Male Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Rats Rats, Inbred Lew Rats, Inbred WKY Viral diseases Viral hepatitis Wistar Kyoto (WKY) rat |
| title | Strain susceptibility to active induction and passive transfer of experimental autoimmune glomerulonephritis in the rat |
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