Back-Pack Mice as a Model of Renal Mesangial IgA Dimers Deposition
Mesangial IgA in IgA nephropathy are dimers with a J chain but no poly-Ig receptor. This molecular structure has led to the hypothesis that these IgA are issued from the lamina propria of mucosal areas, reaching the kidney by way of the peripheral blood. The availability of hybridomas producing IgA...
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| Veröffentlicht in: | International journal of immunopathology and pharmacology 2005-10, Vol.18 (4), p.701-708 |
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| container_title | International journal of immunopathology and pharmacology |
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| creator | March, A. Kennel-De Prin-Mathieu, C. Kohler, C.H. Kolopp-Sarda, M.N. Faure, G.C. Béné, M.C. |
| description | Mesangial IgA in IgA nephropathy are dimers with a J chain but no poly-Ig receptor. This molecular structure has led to the hypothesis that these IgA are issued from the lamina propria of mucosal areas, reaching the kidney by way of the peripheral blood. The availability of hybridomas producing IgA dimers provided an opportunity to test this hypothesis in a new experimental model of IgA nephropathy. Mice were injected subcutaneously (back-pack mice) or intraperitoneally with hybridoma cells secreting either monoclonal IgA dimers, or monoclonal IgA monomers. The influence of immune complex formation was also tested in both these models. Renal IgA deposition was investigated 12 days after the injection of hybridoma cells. Backpack mice developed highly vascularized subcutaneous tumors. Mesangial IgA deposits were observed only in dimeric IgA hybridoma back-pack animals. No significant staining was observed in glomeruli from animals injected with hybridoma cells producing monomeric IgA. None of the hybridomas induced mesangial deposition when injected intraperitoneally. This animal model demonstrates the capacity of circulating IgA dimers to spontaneously form mesangial deposits and contributes to confirm the involvement of abnormalities of mucosal immunity in the pathogenesis of IgA nephropathy. |
| doi_str_mv | 10.1177/039463200501800412 |
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Kennel-De ; Prin-Mathieu, C. ; Kohler, C.H. ; Kolopp-Sarda, M.N. ; Faure, G.C. ; Béné, M.C.</creator><creatorcontrib>March, A. Kennel-De ; Prin-Mathieu, C. ; Kohler, C.H. ; Kolopp-Sarda, M.N. ; Faure, G.C. ; Béné, M.C.</creatorcontrib><description>Mesangial IgA in IgA nephropathy are dimers with a J chain but no poly-Ig receptor. This molecular structure has led to the hypothesis that these IgA are issued from the lamina propria of mucosal areas, reaching the kidney by way of the peripheral blood. The availability of hybridomas producing IgA dimers provided an opportunity to test this hypothesis in a new experimental model of IgA nephropathy. Mice were injected subcutaneously (back-pack mice) or intraperitoneally with hybridoma cells secreting either monoclonal IgA dimers, or monoclonal IgA monomers. The influence of immune complex formation was also tested in both these models. Renal IgA deposition was investigated 12 days after the injection of hybridoma cells. Backpack mice developed highly vascularized subcutaneous tumors. Mesangial IgA deposits were observed only in dimeric IgA hybridoma back-pack animals. No significant staining was observed in glomeruli from animals injected with hybridoma cells producing monomeric IgA. None of the hybridomas induced mesangial deposition when injected intraperitoneally. This animal model demonstrates the capacity of circulating IgA dimers to spontaneously form mesangial deposits and contributes to confirm the involvement of abnormalities of mucosal immunity in the pathogenesis of IgA nephropathy.</description><identifier>ISSN: 0394-6320</identifier><identifier>EISSN: 2058-7384</identifier><identifier>DOI: 10.1177/039463200501800412</identifier><identifier>PMID: 16388718</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Antibodies, Monoclonal - metabolism ; B-Lymphocytes - immunology ; B-Lymphocytes - physiology ; Cell Transplantation ; Fluorescent Antibody Technique ; Glomerular Mesangium - immunology ; Glomerular Mesangium - metabolism ; Glomerulonephritis, IGA - immunology ; Glomerulonephritis, IGA - metabolism ; Hybridomas - immunology ; Hybridomas - transplantation ; Immunoglobulin A - immunology ; Immunoglobulin A - metabolism ; Lymphatic System - immunology ; Lymphatic System - pathology ; Male ; Mice ; Mice, Inbred BALB C ; Palatine Tonsil - immunology ; Palatine Tonsil - pathology ; Plasma Cells - immunology ; Receptors, Lymphocyte Homing - physiology</subject><ispartof>International journal of immunopathology and pharmacology, 2005-10, Vol.18 (4), p.701-708</ispartof><rights>2005 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-3e4998592d4aeb2e0940a9974deffa1b9279c9522aaa7d8b756c5cf15366079d3</citedby><cites>FETCH-LOGICAL-c416t-3e4998592d4aeb2e0940a9974deffa1b9279c9522aaa7d8b756c5cf15366079d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/039463200501800412$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/039463200501800412$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21966,27853,27924,27925,44945,45333</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/039463200501800412?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16388718$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>March, A. 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Mice were injected subcutaneously (back-pack mice) or intraperitoneally with hybridoma cells secreting either monoclonal IgA dimers, or monoclonal IgA monomers. The influence of immune complex formation was also tested in both these models. Renal IgA deposition was investigated 12 days after the injection of hybridoma cells. Backpack mice developed highly vascularized subcutaneous tumors. Mesangial IgA deposits were observed only in dimeric IgA hybridoma back-pack animals. No significant staining was observed in glomeruli from animals injected with hybridoma cells producing monomeric IgA. None of the hybridomas induced mesangial deposition when injected intraperitoneally. This animal model demonstrates the capacity of circulating IgA dimers to spontaneously form mesangial deposits and contributes to confirm the involvement of abnormalities of mucosal immunity in the pathogenesis of IgA nephropathy.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - metabolism</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - physiology</subject><subject>Cell Transplantation</subject><subject>Fluorescent Antibody Technique</subject><subject>Glomerular Mesangium - immunology</subject><subject>Glomerular Mesangium - metabolism</subject><subject>Glomerulonephritis, IGA - immunology</subject><subject>Glomerulonephritis, IGA - metabolism</subject><subject>Hybridomas - immunology</subject><subject>Hybridomas - transplantation</subject><subject>Immunoglobulin A - immunology</subject><subject>Immunoglobulin A - metabolism</subject><subject>Lymphatic System - immunology</subject><subject>Lymphatic System - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Palatine Tonsil - immunology</subject><subject>Palatine Tonsil - pathology</subject><subject>Plasma Cells - immunology</subject><subject>Receptors, Lymphocyte Homing - physiology</subject><issn>0394-6320</issn><issn>2058-7384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkDtPwzAUhS0EolXpH2BAnthC73Xs2B774FGpFQjBHDnJTZWSR4mbgX9PqlZiQILlnjt85wwfY9cId4haTyC0MgoFgAI0ABLFGRsKUCbQoZHnbHgAggMxYGPvtwCAEEpl8JINMAqN0WiGbDZz6Ufw0h--LlLiznPH101GJW9y_kq1K_mavKs3Rf8tN1O-KCpqPV_QrvHFvmjqK3aRu9LT-JQj9v5w_zZ_ClbPj8v5dBWkEqN9EJK01igrMukoEQRWgrNWy4zy3GFihbapVUI453RmEq2iVKU5qjCKQNssHLHb4-6ubT478vu4KnxKZelqajofRxYUWqn_BVEjgkHZg-IIpm3jfUt5vGuLyrVfMUJ8sBz_ttyXbk7rXVJR9lM5Oe2ByRHwbkPxtunaXqL_a_Ibh_qBLw</recordid><startdate>20051001</startdate><enddate>20051001</enddate><creator>March, A. 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Kennel-De</creatorcontrib><creatorcontrib>Prin-Mathieu, C.</creatorcontrib><creatorcontrib>Kohler, C.H.</creatorcontrib><creatorcontrib>Kolopp-Sarda, M.N.</creatorcontrib><creatorcontrib>Faure, G.C.</creatorcontrib><creatorcontrib>Béné, M.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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of immunopathology and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>March, A. Kennel-De</au><au>Prin-Mathieu, C.</au><au>Kohler, C.H.</au><au>Kolopp-Sarda, M.N.</au><au>Faure, G.C.</au><au>Béné, M.C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Back-Pack Mice as a Model of Renal Mesangial IgA Dimers Deposition</atitle><jtitle>International journal of immunopathology and pharmacology</jtitle><addtitle>Int J Immunopathol Pharmacol</addtitle><date>2005-10-01</date><risdate>2005</risdate><volume>18</volume><issue>4</issue><spage>701</spage><epage>708</epage><pages>701-708</pages><issn>0394-6320</issn><eissn>2058-7384</eissn><abstract>Mesangial IgA in IgA nephropathy are dimers with a J chain but no poly-Ig receptor. This molecular structure has led to the hypothesis that these IgA are issued from the lamina propria of mucosal areas, reaching the kidney by way of the peripheral blood. The availability of hybridomas producing IgA dimers provided an opportunity to test this hypothesis in a new experimental model of IgA nephropathy. Mice were injected subcutaneously (back-pack mice) or intraperitoneally with hybridoma cells secreting either monoclonal IgA dimers, or monoclonal IgA monomers. The influence of immune complex formation was also tested in both these models. Renal IgA deposition was investigated 12 days after the injection of hybridoma cells. Backpack mice developed highly vascularized subcutaneous tumors. Mesangial IgA deposits were observed only in dimeric IgA hybridoma back-pack animals. No significant staining was observed in glomeruli from animals injected with hybridoma cells producing monomeric IgA. None of the hybridomas induced mesangial deposition when injected intraperitoneally. 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| subjects | Animals Antibodies, Monoclonal - metabolism B-Lymphocytes - immunology B-Lymphocytes - physiology Cell Transplantation Fluorescent Antibody Technique Glomerular Mesangium - immunology Glomerular Mesangium - metabolism Glomerulonephritis, IGA - immunology Glomerulonephritis, IGA - metabolism Hybridomas - immunology Hybridomas - transplantation Immunoglobulin A - immunology Immunoglobulin A - metabolism Lymphatic System - immunology Lymphatic System - pathology Male Mice Mice, Inbred BALB C Palatine Tonsil - immunology Palatine Tonsil - pathology Plasma Cells - immunology Receptors, Lymphocyte Homing - physiology |
| title | Back-Pack Mice as a Model of Renal Mesangial IgA Dimers Deposition |
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