Th1 and Th17 Cells Induce Proliferative Glomerulonephritis
Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cell...
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| Veröffentlicht in: | Journal of the American Society of Nephrology 2009-12, Vol.20 (12), p.2518-2524 |
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| creator | SUMMERS, Shaun A STEINMETZ, Oliver M MING LI KAUSMAN, Joshua Y SEMPLE, Timothy EDGTTON, Kristy L BORZA, Dorin-Bogdan BRALEY, Hal HOLDSWORTH, Stephen R KITCHING, A. Richard |
| description | Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies. |
| doi_str_mv | 10.1681/asn.2009030337 |
| format | Article |
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Richard</creator><creatorcontrib>SUMMERS, Shaun A ; STEINMETZ, Oliver M ; MING LI ; KAUSMAN, Joshua Y ; SEMPLE, Timothy ; EDGTTON, Kristy L ; BORZA, Dorin-Bogdan ; BRALEY, Hal ; HOLDSWORTH, Stephen R ; KITCHING, A. Richard</creatorcontrib><description>Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/asn.2009030337</identifier><identifier>PMID: 19820122</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Washington, DC: American Society of Nephrology</publisher><subject>Adaptive Immunity ; Adoptive Transfer ; Animals ; Biological and medical sciences ; Brief Communications ; Chemokines - genetics ; Chemokines - metabolism ; Disease Models, Animal ; Genes, RAG-1 ; Glomerulonephritis ; Glomerulonephritis, Membranoproliferative - etiology ; Glomerulonephritis, Membranoproliferative - genetics ; Glomerulonephritis, Membranoproliferative - immunology ; Immunoglobulin G - metabolism ; Interleukin-17 - metabolism ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Ovalbumin - immunology ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; T-Lymphocyte Subsets - immunology ; T-Lymphocytes, Helper-Inducer - immunology ; Th1 Cells - immunology</subject><ispartof>Journal of the American Society of Nephrology, 2009-12, Vol.20 (12), p.2518-2524</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright © 2009 by the American Society of Nephrology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-4fc7fcdfa22afb7bdedf9d96bcc52df2c51017b57d0a5e768e35059910b708723</citedby><cites>FETCH-LOGICAL-c485t-4fc7fcdfa22afb7bdedf9d96bcc52df2c51017b57d0a5e768e35059910b708723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2794236/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2794236/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22176722$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19820122$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SUMMERS, Shaun A</creatorcontrib><creatorcontrib>STEINMETZ, Oliver M</creatorcontrib><creatorcontrib>MING LI</creatorcontrib><creatorcontrib>KAUSMAN, Joshua Y</creatorcontrib><creatorcontrib>SEMPLE, Timothy</creatorcontrib><creatorcontrib>EDGTTON, Kristy L</creatorcontrib><creatorcontrib>BORZA, Dorin-Bogdan</creatorcontrib><creatorcontrib>BRALEY, Hal</creatorcontrib><creatorcontrib>HOLDSWORTH, Stephen R</creatorcontrib><creatorcontrib>KITCHING, A. Richard</creatorcontrib><title>Th1 and Th17 Cells Induce Proliferative Glomerulonephritis</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.</description><subject>Adaptive Immunity</subject><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brief Communications</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Genes, RAG-1</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis, Membranoproliferative - etiology</subject><subject>Glomerulonephritis, Membranoproliferative - genetics</subject><subject>Glomerulonephritis, Membranoproliferative - immunology</subject><subject>Immunoglobulin G - metabolism</subject><subject>Interleukin-17 - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Ovalbumin - immunology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>Th1 Cells - immunology</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkM1LAzEQxYMotlavHmUv4mlrPjabjQehFK2FooL1HLL5sJHtbk12C_73Rrq0enoD85s3Mw-ASwTHKC_QrQz1GEPIIYGEsCMwRJSQlGQUHscaZnma54wMwFkInxAiihk7BQPECwwRxkNwt1yhRNY6icqSqamqkMxr3SmTvPqmctZ42bqtSWZVsza-q5rabFbetS6cgxMrq2Aueh2B98eH5fQpXbzM5tPJIlVZQds0s4pZpa3EWNqSldpoyzXPS6Uo1hYriiBiJWUaSmpYXhhCIeUcwZLBgmEyAvc7301Xro1Wpm69rMTGu7X036KRTvzv1G4lPpqtwIxnmOTR4KY38M1XZ0Ir1i6o-KqsTdMFwQghBY-ZRHK8I5VvQvDG7rcgKH7zFpO3Z3HIOw5c_b3tgPcBR-C6B2RQsrJe1sqFPYcxYjmL3A8X8Ija</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>SUMMERS, Shaun A</creator><creator>STEINMETZ, Oliver M</creator><creator>MING LI</creator><creator>KAUSMAN, Joshua Y</creator><creator>SEMPLE, Timothy</creator><creator>EDGTTON, Kristy L</creator><creator>BORZA, Dorin-Bogdan</creator><creator>BRALEY, Hal</creator><creator>HOLDSWORTH, Stephen R</creator><creator>KITCHING, A. Richard</creator><general>American Society of Nephrology</general><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>5PM</scope></search><sort><creationdate>20091201</creationdate><title>Th1 and Th17 Cells Induce Proliferative Glomerulonephritis</title><author>SUMMERS, Shaun A ; STEINMETZ, Oliver M ; MING LI ; KAUSMAN, Joshua Y ; SEMPLE, Timothy ; EDGTTON, Kristy L ; BORZA, Dorin-Bogdan ; BRALEY, Hal ; HOLDSWORTH, Stephen R ; KITCHING, A. Richard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-4fc7fcdfa22afb7bdedf9d96bcc52df2c51017b57d0a5e768e35059910b708723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adaptive Immunity</topic><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brief Communications</topic><topic>Chemokines - genetics</topic><topic>Chemokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Genes, RAG-1</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis, Membranoproliferative - etiology</topic><topic>Glomerulonephritis, Membranoproliferative - genetics</topic><topic>Glomerulonephritis, Membranoproliferative - immunology</topic><topic>Immunoglobulin G - metabolism</topic><topic>Interleukin-17 - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Ovalbumin - immunology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>Th1 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SUMMERS, Shaun A</creatorcontrib><creatorcontrib>STEINMETZ, Oliver M</creatorcontrib><creatorcontrib>MING LI</creatorcontrib><creatorcontrib>KAUSMAN, Joshua Y</creatorcontrib><creatorcontrib>SEMPLE, Timothy</creatorcontrib><creatorcontrib>EDGTTON, Kristy L</creatorcontrib><creatorcontrib>BORZA, Dorin-Bogdan</creatorcontrib><creatorcontrib>BRALEY, Hal</creatorcontrib><creatorcontrib>HOLDSWORTH, Stephen R</creatorcontrib><creatorcontrib>KITCHING, A. Richard</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SUMMERS, Shaun A</au><au>STEINMETZ, Oliver M</au><au>MING LI</au><au>KAUSMAN, Joshua Y</au><au>SEMPLE, Timothy</au><au>EDGTTON, Kristy L</au><au>BORZA, Dorin-Bogdan</au><au>BRALEY, Hal</au><au>HOLDSWORTH, Stephen R</au><au>KITCHING, A. Richard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Th1 and Th17 Cells Induce Proliferative Glomerulonephritis</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>20</volume><issue>12</issue><spage>2518</spage><epage>2524</epage><pages>2518-2524</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>Th1 effector CD4+ cells contribute to the pathogenesis of proliferative and crescentic glomerulonephritis, but whether effector Th17 cells also contribute is unknown. We compared the involvement of Th1 and Th17 cells in a mouse model of antigen-specific glomerulonephritis in which effector CD4+ cells are the only components of adaptive immunity that induce injury. We planted the antigen ovalbumin on the glomerular basement membrane of Rag1(-/-) mice using an ovalbumin-conjugated non-nephritogenic IgG1 monoclonal antibody against alpha3(IV) collagen. Subsequent injection of either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells induced proliferative glomerulonephritis. Mice injected with Th1 cells developed progressive albuminuria over 21 d, histologic injury including 5.5 +/- 0.9% crescent formation/segmental necrosis, elevated urinary nitrate, and increased renal NOS2, CCL2, and CCL5 mRNA. Mice injected with Th17 cells developed albuminuria by 3 d; compared with Th1-injected mice, their glomeruli contained more neutrophils and greater expression of renal CXCL1 mRNA. In conclusion, Th1 and Th17 effector cells can induce glomerular injury. Understanding how these two subsets mediate proliferative forms of glomerulonephritis may lead to targeted therapies.</abstract><cop>Washington, DC</cop><pub>American Society of Nephrology</pub><pmid>19820122</pmid><doi>10.1681/asn.2009030337</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptive Immunity Adoptive Transfer Animals Biological and medical sciences Brief Communications Chemokines - genetics Chemokines - metabolism Disease Models, Animal Genes, RAG-1 Glomerulonephritis Glomerulonephritis, Membranoproliferative - etiology Glomerulonephritis, Membranoproliferative - genetics Glomerulonephritis, Membranoproliferative - immunology Immunoglobulin G - metabolism Interleukin-17 - metabolism Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Ovalbumin - immunology RNA, Messenger - genetics RNA, Messenger - metabolism T-Lymphocyte Subsets - immunology T-Lymphocytes, Helper-Inducer - immunology Th1 Cells - immunology |
| title | Th1 and Th17 Cells Induce Proliferative Glomerulonephritis |
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