Chronic rejection of mouse kidney allografts
Chronic rejection of mouse kidney allografts. Chronic renal allograft rejection is the leading cause of late graft failure. However, its pathogenesis has not been defined. To explore the pathogenesis of chronic rejection, we studied a mouse model of kidney transplantation and examined the effects of...
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| Veröffentlicht in: | Kidney international 1999-05, Vol.55 (5), p.1935-1944 |
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| creator | Mannon, Roslyn B. Kopp, Jeffrey B. Ruiz, Philip Griffiths, Robert Bustos, Matilde Platt, Jeffrey L. Klotman, Paul E. Coffman, Thomas M. |
| description | Chronic rejection of mouse kidney allografts.
Chronic renal allograft rejection is the leading cause of late graft failure. However, its pathogenesis has not been defined.
To explore the pathogenesis of chronic rejection, we studied a mouse model of kidney transplantation and examined the effects of altering the expression of donor major histocompatibility complex (MHC) antigens on the development of chronic rejection.
We found that long-surviving mouse kidney allografts develop pathological abnormalities that resemble chronic rejection in humans. Furthermore, the absence of MHC class I or class II antigens did not prevent the loss of graft function nor alter the pathological characteristics of chronic rejection. Expression of transforming growth factor-β (TGF-β), a pleiotropic cytokine suggested to play a role in chronic rejection, was markedly enhanced in control allografts compared with isografts. However, TGF-β up-regulation was significantly blunted in MHC-deficient grafts. Nonetheless, these differences in TGF-β expression did not affect the character of chronic rejection, including intrarenal accumulation of collagens.
Reduced expression of either class I or II direct allorecognition pathways is insufficient to prevent the development of chronic rejection, despite a reduction in the levels of TGF-β expressed in the allograft. This suggests that the severity of chronic rejection is independent of the level of MHC disparity between donor and recipient and the level of TGF-β expression within the allograft. |
| doi_str_mv | 10.1046/j.1523-1755.1999.00423.x |
| format | Article |
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Chronic renal allograft rejection is the leading cause of late graft failure. However, its pathogenesis has not been defined.
To explore the pathogenesis of chronic rejection, we studied a mouse model of kidney transplantation and examined the effects of altering the expression of donor major histocompatibility complex (MHC) antigens on the development of chronic rejection.
We found that long-surviving mouse kidney allografts develop pathological abnormalities that resemble chronic rejection in humans. Furthermore, the absence of MHC class I or class II antigens did not prevent the loss of graft function nor alter the pathological characteristics of chronic rejection. Expression of transforming growth factor-β (TGF-β), a pleiotropic cytokine suggested to play a role in chronic rejection, was markedly enhanced in control allografts compared with isografts. However, TGF-β up-regulation was significantly blunted in MHC-deficient grafts. Nonetheless, these differences in TGF-β expression did not affect the character of chronic rejection, including intrarenal accumulation of collagens.
Reduced expression of either class I or II direct allorecognition pathways is insufficient to prevent the development of chronic rejection, despite a reduction in the levels of TGF-β expressed in the allograft. This suggests that the severity of chronic rejection is independent of the level of MHC disparity between donor and recipient and the level of TGF-β expression within the allograft.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.1999.00423.x</identifier><identifier>PMID: 10231457</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; arteriosclerosis ; Biological and medical sciences ; Blotting, Northern ; Chronic Disease ; Collagen - analysis ; Collagen - immunology ; fibrosis ; Gene Expression ; Glomerular Filtration Rate ; glomerulosclerosis ; Graft Rejection - immunology ; Histocompatibility Antigens Class I - analysis ; Histocompatibility Antigens Class I - immunology ; Histocompatibility Antigens Class II - analysis ; Histocompatibility Antigens Class II - immunology ; Immunoenzyme Techniques ; Isoantigens - analysis ; Isoantigens - immunology ; Kidney - chemistry ; Kidney - immunology ; Kidney - physiology ; Kidney Transplantation ; Kidneys ; Lymphocytes - immunology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; mouse MHC ; Nephrology. Urinary tract diseases ; renal graft rejection ; RNA, Messenger - analysis ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the urinary system ; TGF-β ; Transforming Growth Factor beta - analysis ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - immunology ; transplantation ; Transplantation Immunology - immunology ; Transplantation, Homologous ; Urinary system involvement in other diseases. Miscellaneous</subject><ispartof>Kidney international, 1999-05, Vol.55 (5), p.1935-1944</ispartof><rights>1999 International Society of Nephrology</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-a9dd66f7ed969c2696434d94079ddb79b0204ffa2cd8195d9acdd5c445981d0c3</citedby><cites>FETCH-LOGICAL-c449t-a9dd66f7ed969c2696434d94079ddb79b0204ffa2cd8195d9acdd5c445981d0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,23909,23910,25118,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1781398$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10231457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mannon, Roslyn B.</creatorcontrib><creatorcontrib>Kopp, Jeffrey B.</creatorcontrib><creatorcontrib>Ruiz, Philip</creatorcontrib><creatorcontrib>Griffiths, Robert</creatorcontrib><creatorcontrib>Bustos, Matilde</creatorcontrib><creatorcontrib>Platt, Jeffrey L.</creatorcontrib><creatorcontrib>Klotman, Paul E.</creatorcontrib><creatorcontrib>Coffman, Thomas M.</creatorcontrib><title>Chronic rejection of mouse kidney allografts</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Chronic rejection of mouse kidney allografts.
Chronic renal allograft rejection is the leading cause of late graft failure. However, its pathogenesis has not been defined.
To explore the pathogenesis of chronic rejection, we studied a mouse model of kidney transplantation and examined the effects of altering the expression of donor major histocompatibility complex (MHC) antigens on the development of chronic rejection.
We found that long-surviving mouse kidney allografts develop pathological abnormalities that resemble chronic rejection in humans. Furthermore, the absence of MHC class I or class II antigens did not prevent the loss of graft function nor alter the pathological characteristics of chronic rejection. Expression of transforming growth factor-β (TGF-β), a pleiotropic cytokine suggested to play a role in chronic rejection, was markedly enhanced in control allografts compared with isografts. However, TGF-β up-regulation was significantly blunted in MHC-deficient grafts. Nonetheless, these differences in TGF-β expression did not affect the character of chronic rejection, including intrarenal accumulation of collagens.
Reduced expression of either class I or II direct allorecognition pathways is insufficient to prevent the development of chronic rejection, despite a reduction in the levels of TGF-β expressed in the allograft. This suggests that the severity of chronic rejection is independent of the level of MHC disparity between donor and recipient and the level of TGF-β expression within the allograft.</description><subject>Animals</subject><subject>arteriosclerosis</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Chronic Disease</subject><subject>Collagen - analysis</subject><subject>Collagen - immunology</subject><subject>fibrosis</subject><subject>Gene Expression</subject><subject>Glomerular Filtration Rate</subject><subject>glomerulosclerosis</subject><subject>Graft Rejection - immunology</subject><subject>Histocompatibility Antigens Class I - analysis</subject><subject>Histocompatibility Antigens Class I - immunology</subject><subject>Histocompatibility Antigens Class II - analysis</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Immunoenzyme Techniques</subject><subject>Isoantigens - analysis</subject><subject>Isoantigens - immunology</subject><subject>Kidney - chemistry</subject><subject>Kidney - immunology</subject><subject>Kidney - physiology</subject><subject>Kidney Transplantation</subject><subject>Kidneys</subject><subject>Lymphocytes - immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>mouse MHC</subject><subject>Nephrology. Urinary tract diseases</subject><subject>renal graft rejection</subject><subject>RNA, Messenger - analysis</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the urinary system</subject><subject>TGF-β</subject><subject>Transforming Growth Factor beta - analysis</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - immunology</subject><subject>transplantation</subject><subject>Transplantation Immunology - immunology</subject><subject>Transplantation, Homologous</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>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMlOwzAURS0EoqXwCygLxIoEj3G8hIpJQmIDa8v1AA4Zip2i9u9xaAXsWFlP79znqwNAhmCBIC0v6wIxTHLEGSuQEKKAkGJSrPfA9GexD6YQVizHjFQTcBRjDdMsCDwEEwQxQZTxKbiYv4W-8zoLtrZ68H2X9S5r-1W02bs3nd1kqmn616DcEI_BgVNNtCe7dwZebm-e5_f549Pdw_zqMdeUiiFXwpiydNwaUQqNS1FSQo2gkKfFgosFxJA6p7A2FRLMCKWNYSnLRIUM1GQGzrd3l6H_WNk4yNZHbZtGdTY1k6XgFHNcJbDagjr0MQbr5DL4VoWNRFCOpmQtRyFyFCJHU_LblFyn6Onuj9WiteZPcKsmAWc7QEWtGhdUp3385XiFiBgrXG8xm4R8ehtk1N522hofklBpev9_mS9CzIZQ</recordid><startdate>19990501</startdate><enddate>19990501</enddate><creator>Mannon, Roslyn B.</creator><creator>Kopp, Jeffrey B.</creator><creator>Ruiz, Philip</creator><creator>Griffiths, Robert</creator><creator>Bustos, Matilde</creator><creator>Platt, Jeffrey L.</creator><creator>Klotman, Paul E.</creator><creator>Coffman, Thomas M.</creator><general>Elsevier Inc</general><general>Nature Publishing</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>7X8</scope></search><sort><creationdate>19990501</creationdate><title>Chronic rejection of mouse kidney allografts</title><author>Mannon, Roslyn B. ; Kopp, Jeffrey B. ; Ruiz, Philip ; Griffiths, Robert ; Bustos, Matilde ; Platt, Jeffrey L. ; Klotman, Paul E. ; Coffman, Thomas M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-a9dd66f7ed969c2696434d94079ddb79b0204ffa2cd8195d9acdd5c445981d0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>arteriosclerosis</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Chronic Disease</topic><topic>Collagen - analysis</topic><topic>Collagen - immunology</topic><topic>fibrosis</topic><topic>Gene Expression</topic><topic>Glomerular Filtration Rate</topic><topic>glomerulosclerosis</topic><topic>Graft Rejection - immunology</topic><topic>Histocompatibility Antigens Class I - analysis</topic><topic>Histocompatibility Antigens Class I - immunology</topic><topic>Histocompatibility Antigens Class II - analysis</topic><topic>Histocompatibility Antigens Class II - immunology</topic><topic>Immunoenzyme Techniques</topic><topic>Isoantigens - analysis</topic><topic>Isoantigens - immunology</topic><topic>Kidney - chemistry</topic><topic>Kidney - immunology</topic><topic>Kidney - physiology</topic><topic>Kidney Transplantation</topic><topic>Kidneys</topic><topic>Lymphocytes - immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>mouse MHC</topic><topic>Nephrology. Urinary tract diseases</topic><topic>renal graft rejection</topic><topic>RNA, Messenger - analysis</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the urinary system</topic><topic>TGF-β</topic><topic>Transforming Growth Factor beta - analysis</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - immunology</topic><topic>transplantation</topic><topic>Transplantation Immunology - immunology</topic><topic>Transplantation, Homologous</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mannon, Roslyn B.</creatorcontrib><creatorcontrib>Kopp, Jeffrey B.</creatorcontrib><creatorcontrib>Ruiz, Philip</creatorcontrib><creatorcontrib>Griffiths, Robert</creatorcontrib><creatorcontrib>Bustos, Matilde</creatorcontrib><creatorcontrib>Platt, Jeffrey L.</creatorcontrib><creatorcontrib>Klotman, Paul E.</creatorcontrib><creatorcontrib>Coffman, Thomas M.</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>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mannon, Roslyn B.</au><au>Kopp, Jeffrey B.</au><au>Ruiz, Philip</au><au>Griffiths, Robert</au><au>Bustos, Matilde</au><au>Platt, Jeffrey L.</au><au>Klotman, Paul E.</au><au>Coffman, Thomas M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic rejection of mouse kidney allografts</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1999-05-01</date><risdate>1999</risdate><volume>55</volume><issue>5</issue><spage>1935</spage><epage>1944</epage><pages>1935-1944</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Chronic rejection of mouse kidney allografts.
Chronic renal allograft rejection is the leading cause of late graft failure. However, its pathogenesis has not been defined.
To explore the pathogenesis of chronic rejection, we studied a mouse model of kidney transplantation and examined the effects of altering the expression of donor major histocompatibility complex (MHC) antigens on the development of chronic rejection.
We found that long-surviving mouse kidney allografts develop pathological abnormalities that resemble chronic rejection in humans. Furthermore, the absence of MHC class I or class II antigens did not prevent the loss of graft function nor alter the pathological characteristics of chronic rejection. Expression of transforming growth factor-β (TGF-β), a pleiotropic cytokine suggested to play a role in chronic rejection, was markedly enhanced in control allografts compared with isografts. However, TGF-β up-regulation was significantly blunted in MHC-deficient grafts. Nonetheless, these differences in TGF-β expression did not affect the character of chronic rejection, including intrarenal accumulation of collagens.
Reduced expression of either class I or II direct allorecognition pathways is insufficient to prevent the development of chronic rejection, despite a reduction in the levels of TGF-β expressed in the allograft. This suggests that the severity of chronic rejection is independent of the level of MHC disparity between donor and recipient and the level of TGF-β expression within the allograft.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10231457</pmid><doi>10.1046/j.1523-1755.1999.00423.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 1999-05, Vol.55 (5), p.1935-1944 |
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| subjects | Animals arteriosclerosis Biological and medical sciences Blotting, Northern Chronic Disease Collagen - analysis Collagen - immunology fibrosis Gene Expression Glomerular Filtration Rate glomerulosclerosis Graft Rejection - immunology Histocompatibility Antigens Class I - analysis Histocompatibility Antigens Class I - immunology Histocompatibility Antigens Class II - analysis Histocompatibility Antigens Class II - immunology Immunoenzyme Techniques Isoantigens - analysis Isoantigens - immunology Kidney - chemistry Kidney - immunology Kidney - physiology Kidney Transplantation Kidneys Lymphocytes - immunology Medical sciences Mice Mice, Inbred C57BL mouse MHC Nephrology. Urinary tract diseases renal graft rejection RNA, Messenger - analysis Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the urinary system TGF-β Transforming Growth Factor beta - analysis Transforming Growth Factor beta - genetics Transforming Growth Factor beta - immunology transplantation Transplantation Immunology - immunology Transplantation, Homologous Urinary system involvement in other diseases. Miscellaneous |
| title | Chronic rejection of mouse kidney allografts |
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