Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis
Objective The CD4+ T cell immune response plays a pivotal role in the immunopathogenesis of human and experimental lupus nephritis, but the contribution of the Th17/interleukin‐17 (IL‐17) immune pathway to renal tissue injury in systemic lupus erythematosus (SLE) remains to be elucidated. The aim of...
Gespeichert in:
| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2015-02, Vol.67 (2), p.475-487 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 487 |
|---|---|
| container_issue | 2 |
| container_start_page | 475 |
| container_title | Arthritis & rheumatology (Hoboken, N.J.) |
| container_volume | 67 |
| creator | Schmidt, Tilman Paust, Hans‐Joachim Krebs, Christian F. Turner, Jan‐Eric Kaffke, Anna Bennstein, Sabrina B. Koyro, Tobias Peters, Anett Velden, Joachim Hünemörder, Stefanie Haag, Friedrich Steinmetz, Oliver M. Mittrücker, Hans‐Willi Stahl, Rolf A. K. Panzer, Ulf |
| description | Objective
The CD4+ T cell immune response plays a pivotal role in the immunopathogenesis of human and experimental lupus nephritis, but the contribution of the Th17/interleukin‐17 (IL‐17) immune pathway to renal tissue injury in systemic lupus erythematosus (SLE) remains to be elucidated. The aim of this study was to characterize the function of the Th17/IL‐17A immune response in 2 murine models of lupus nephritis.
Methods
IL‐17A–deficient MRL/MPJ‐Faslpr/2J (MRL/lpr) mice were generated, and the clinical course of nephritis was monitored by assessing the levels of albuminuria, extent of renal tissue injury, and functional parameters. In addition, lupus‐prone (NZB × NZW)F1 (NZB/NZW) mice were treated with anti–IL‐17A and anti–interferon‐γ (anti‐IFNγ) antibodies, and their effects on the clinical course of lupus nephritis were assessed.
Results
Characterization of renal IL‐17A–producing and IFNγ‐producing T cells in MRL/lpr and NZB/NZW mice revealed low numbers of infiltrating CD3+IL‐17A+ cells. Renal IL‐17A was mainly produced by CD4/CD8 double‐negative CD3+ T cells and CD4+ Th17 cells. In contrast, the number of renal CD3+IFNγ+ cells continuously increased over time and largely consisted of typical CD4+ Th1 cells. IL‐17A deficiency did not affect the morphologic or functional parameters in MRL/lpr mice with lupus nephritis, nor did IL‐17A neutralization affect the clinical course of nephritis in NZB/NZW mice, but anti‐IFNγ treatment attenuated the severity of the disease.
Conclusion
The Th17/IL‐17A immune response plays no major role in the immunopathogenesis of lupus nephritis in MRL/lpr and NZB/NZW mice. Thus, the results of this study do not support the hypothesis that IL‐17A targeting could be an intriguing new therapeutic approach for the management of proliferative lupus nephritis in SLE patients. |
| doi_str_mv | 10.1002/art.38955 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1660429600</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3571032751</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3865-f331c959a55e9aaf1f7059f40963a5516c236d270c4c3146a51900416b0e33df3</originalsourceid><addsrcrecordid>eNqN0ctKAzEUBuAgioq68AVkwI0uak8uJ9Msi1gt1AulrofpNEOjM5kxmSDufASf0ScxtepCEMzmhMPHD4efkEMKZxSA9XPXnfGBQtwgu4wz2UMGuPn9p4rukAPvHyA-lYIE3CY7DPkAEWGX3I2CLTrT2KQpk26pk9mSpv2x7bSrdHg09v31jabDZFzXwepkqn3bWK8TY5Pr4ExcTUIbfHKj26UznfH7ZKvMK68PvuYeuR9dzM6vepPby_H5cNIr-EBir-ScFgpVjqhVnpe0TAFVKUBJHndUFozLBUuhEAWnQubxEgBB5Rw054uS75GTdW7rmqegfZfVxhe6qnKrm-AzKiUIpiTAPygywQRnK3r8iz40wdl4SFRigApFulKna1W4xnuny6x1ps7dS0YhW5WSxVKyz1KiPfpKDPNaL37kdwUR9Nfg2VT65e-kbDidrSM_AGfqkug</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1648595470</pqid></control><display><type>article</type><title>Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Alma/SFX Local Collection</source><creator>Schmidt, Tilman ; Paust, Hans‐Joachim ; Krebs, Christian F. ; Turner, Jan‐Eric ; Kaffke, Anna ; Bennstein, Sabrina B. ; Koyro, Tobias ; Peters, Anett ; Velden, Joachim ; Hünemörder, Stefanie ; Haag, Friedrich ; Steinmetz, Oliver M. ; Mittrücker, Hans‐Willi ; Stahl, Rolf A. K. ; Panzer, Ulf</creator><creatorcontrib>Schmidt, Tilman ; Paust, Hans‐Joachim ; Krebs, Christian F. ; Turner, Jan‐Eric ; Kaffke, Anna ; Bennstein, Sabrina B. ; Koyro, Tobias ; Peters, Anett ; Velden, Joachim ; Hünemörder, Stefanie ; Haag, Friedrich ; Steinmetz, Oliver M. ; Mittrücker, Hans‐Willi ; Stahl, Rolf A. K. ; Panzer, Ulf</creatorcontrib><description>Objective
The CD4+ T cell immune response plays a pivotal role in the immunopathogenesis of human and experimental lupus nephritis, but the contribution of the Th17/interleukin‐17 (IL‐17) immune pathway to renal tissue injury in systemic lupus erythematosus (SLE) remains to be elucidated. The aim of this study was to characterize the function of the Th17/IL‐17A immune response in 2 murine models of lupus nephritis.
Methods
IL‐17A–deficient MRL/MPJ‐Faslpr/2J (MRL/lpr) mice were generated, and the clinical course of nephritis was monitored by assessing the levels of albuminuria, extent of renal tissue injury, and functional parameters. In addition, lupus‐prone (NZB × NZW)F1 (NZB/NZW) mice were treated with anti–IL‐17A and anti–interferon‐γ (anti‐IFNγ) antibodies, and their effects on the clinical course of lupus nephritis were assessed.
Results
Characterization of renal IL‐17A–producing and IFNγ‐producing T cells in MRL/lpr and NZB/NZW mice revealed low numbers of infiltrating CD3+IL‐17A+ cells. Renal IL‐17A was mainly produced by CD4/CD8 double‐negative CD3+ T cells and CD4+ Th17 cells. In contrast, the number of renal CD3+IFNγ+ cells continuously increased over time and largely consisted of typical CD4+ Th1 cells. IL‐17A deficiency did not affect the morphologic or functional parameters in MRL/lpr mice with lupus nephritis, nor did IL‐17A neutralization affect the clinical course of nephritis in NZB/NZW mice, but anti‐IFNγ treatment attenuated the severity of the disease.
Conclusion
The Th17/IL‐17A immune response plays no major role in the immunopathogenesis of lupus nephritis in MRL/lpr and NZB/NZW mice. Thus, the results of this study do not support the hypothesis that IL‐17A targeting could be an intriguing new therapeutic approach for the management of proliferative lupus nephritis in SLE patients.</description><identifier>ISSN: 2326-5191</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.38955</identifier><identifier>PMID: 25385550</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Antibodies, Anti-Idiotypic - pharmacology ; CD3 Complex - metabolism ; Disease Models, Animal ; Female ; Immunity, Cellular - immunology ; Immunity, Cellular - physiology ; Interferon-gamma - antagonists & inhibitors ; Interferon-gamma - immunology ; Interferon-gamma - physiology ; Interleukin-17 - antagonists & inhibitors ; Interleukin-17 - immunology ; Interleukin-17 - physiology ; Lupus Nephritis - immunology ; Lupus Nephritis - pathology ; Lupus Nephritis - physiopathology ; Male ; Mice ; Mice, Inbred MRL lpr ; Mice, Inbred NZB ; Mice, Knockout ; Severity of Illness Index ; T-Lymphocytes - pathology ; T-Lymphocytes - physiology ; Th17 Cells - pathology ; Th17 Cells - physiology</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2015-02, Vol.67 (2), p.475-487</ispartof><rights>Copyright © 2015 by the American College of Rheumatology</rights><rights>Copyright © 2015 by the American College of Rheumatology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3865-f331c959a55e9aaf1f7059f40963a5516c236d270c4c3146a51900416b0e33df3</citedby><cites>FETCH-LOGICAL-c3865-f331c959a55e9aaf1f7059f40963a5516c236d270c4c3146a51900416b0e33df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fart.38955$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.38955$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25385550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schmidt, Tilman</creatorcontrib><creatorcontrib>Paust, Hans‐Joachim</creatorcontrib><creatorcontrib>Krebs, Christian F.</creatorcontrib><creatorcontrib>Turner, Jan‐Eric</creatorcontrib><creatorcontrib>Kaffke, Anna</creatorcontrib><creatorcontrib>Bennstein, Sabrina B.</creatorcontrib><creatorcontrib>Koyro, Tobias</creatorcontrib><creatorcontrib>Peters, Anett</creatorcontrib><creatorcontrib>Velden, Joachim</creatorcontrib><creatorcontrib>Hünemörder, Stefanie</creatorcontrib><creatorcontrib>Haag, Friedrich</creatorcontrib><creatorcontrib>Steinmetz, Oliver M.</creatorcontrib><creatorcontrib>Mittrücker, Hans‐Willi</creatorcontrib><creatorcontrib>Stahl, Rolf A. K.</creatorcontrib><creatorcontrib>Panzer, Ulf</creatorcontrib><title>Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>Objective
The CD4+ T cell immune response plays a pivotal role in the immunopathogenesis of human and experimental lupus nephritis, but the contribution of the Th17/interleukin‐17 (IL‐17) immune pathway to renal tissue injury in systemic lupus erythematosus (SLE) remains to be elucidated. The aim of this study was to characterize the function of the Th17/IL‐17A immune response in 2 murine models of lupus nephritis.
Methods
IL‐17A–deficient MRL/MPJ‐Faslpr/2J (MRL/lpr) mice were generated, and the clinical course of nephritis was monitored by assessing the levels of albuminuria, extent of renal tissue injury, and functional parameters. In addition, lupus‐prone (NZB × NZW)F1 (NZB/NZW) mice were treated with anti–IL‐17A and anti–interferon‐γ (anti‐IFNγ) antibodies, and their effects on the clinical course of lupus nephritis were assessed.
Results
Characterization of renal IL‐17A–producing and IFNγ‐producing T cells in MRL/lpr and NZB/NZW mice revealed low numbers of infiltrating CD3+IL‐17A+ cells. Renal IL‐17A was mainly produced by CD4/CD8 double‐negative CD3+ T cells and CD4+ Th17 cells. In contrast, the number of renal CD3+IFNγ+ cells continuously increased over time and largely consisted of typical CD4+ Th1 cells. IL‐17A deficiency did not affect the morphologic or functional parameters in MRL/lpr mice with lupus nephritis, nor did IL‐17A neutralization affect the clinical course of nephritis in NZB/NZW mice, but anti‐IFNγ treatment attenuated the severity of the disease.
Conclusion
The Th17/IL‐17A immune response plays no major role in the immunopathogenesis of lupus nephritis in MRL/lpr and NZB/NZW mice. Thus, the results of this study do not support the hypothesis that IL‐17A targeting could be an intriguing new therapeutic approach for the management of proliferative lupus nephritis in SLE patients.</description><subject>Animals</subject><subject>Antibodies, Anti-Idiotypic - pharmacology</subject><subject>CD3 Complex - metabolism</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Immunity, Cellular - immunology</subject><subject>Immunity, Cellular - physiology</subject><subject>Interferon-gamma - antagonists & inhibitors</subject><subject>Interferon-gamma - immunology</subject><subject>Interferon-gamma - physiology</subject><subject>Interleukin-17 - antagonists & inhibitors</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-17 - physiology</subject><subject>Lupus Nephritis - immunology</subject><subject>Lupus Nephritis - pathology</subject><subject>Lupus Nephritis - physiopathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr</subject><subject>Mice, Inbred NZB</subject><subject>Mice, Knockout</subject><subject>Severity of Illness Index</subject><subject>T-Lymphocytes - pathology</subject><subject>T-Lymphocytes - physiology</subject><subject>Th17 Cells - pathology</subject><subject>Th17 Cells - physiology</subject><issn>2326-5191</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0ctKAzEUBuAgioq68AVkwI0uak8uJ9Msi1gt1AulrofpNEOjM5kxmSDufASf0ScxtepCEMzmhMPHD4efkEMKZxSA9XPXnfGBQtwgu4wz2UMGuPn9p4rukAPvHyA-lYIE3CY7DPkAEWGX3I2CLTrT2KQpk26pk9mSpv2x7bSrdHg09v31jabDZFzXwepkqn3bWK8TY5Pr4ExcTUIbfHKj26UznfH7ZKvMK68PvuYeuR9dzM6vepPby_H5cNIr-EBir-ScFgpVjqhVnpe0TAFVKUBJHndUFozLBUuhEAWnQubxEgBB5Rw054uS75GTdW7rmqegfZfVxhe6qnKrm-AzKiUIpiTAPygywQRnK3r8iz40wdl4SFRigApFulKna1W4xnuny6x1ps7dS0YhW5WSxVKyz1KiPfpKDPNaL37kdwUR9Nfg2VT65e-kbDidrSM_AGfqkug</recordid><startdate>201502</startdate><enddate>201502</enddate><creator>Schmidt, Tilman</creator><creator>Paust, Hans‐Joachim</creator><creator>Krebs, Christian F.</creator><creator>Turner, Jan‐Eric</creator><creator>Kaffke, Anna</creator><creator>Bennstein, Sabrina B.</creator><creator>Koyro, Tobias</creator><creator>Peters, Anett</creator><creator>Velden, Joachim</creator><creator>Hünemörder, Stefanie</creator><creator>Haag, Friedrich</creator><creator>Steinmetz, Oliver M.</creator><creator>Mittrücker, Hans‐Willi</creator><creator>Stahl, Rolf A. K.</creator><creator>Panzer, Ulf</creator><general>Wiley Subscription Services, Inc</general><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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201502</creationdate><title>Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis</title><author>Schmidt, Tilman ; Paust, Hans‐Joachim ; Krebs, Christian F. ; Turner, Jan‐Eric ; Kaffke, Anna ; Bennstein, Sabrina B. ; Koyro, Tobias ; Peters, Anett ; Velden, Joachim ; Hünemörder, Stefanie ; Haag, Friedrich ; Steinmetz, Oliver M. ; Mittrücker, Hans‐Willi ; Stahl, Rolf A. K. ; Panzer, Ulf</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3865-f331c959a55e9aaf1f7059f40963a5516c236d270c4c3146a51900416b0e33df3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antibodies, Anti-Idiotypic - pharmacology</topic><topic>CD3 Complex - metabolism</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Immunity, Cellular - immunology</topic><topic>Immunity, Cellular - physiology</topic><topic>Interferon-gamma - antagonists & inhibitors</topic><topic>Interferon-gamma - immunology</topic><topic>Interferon-gamma - physiology</topic><topic>Interleukin-17 - antagonists & inhibitors</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-17 - physiology</topic><topic>Lupus Nephritis - immunology</topic><topic>Lupus Nephritis - pathology</topic><topic>Lupus Nephritis - physiopathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred MRL lpr</topic><topic>Mice, Inbred NZB</topic><topic>Mice, Knockout</topic><topic>Severity of Illness Index</topic><topic>T-Lymphocytes - pathology</topic><topic>T-Lymphocytes - physiology</topic><topic>Th17 Cells - pathology</topic><topic>Th17 Cells - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schmidt, Tilman</creatorcontrib><creatorcontrib>Paust, Hans‐Joachim</creatorcontrib><creatorcontrib>Krebs, Christian F.</creatorcontrib><creatorcontrib>Turner, Jan‐Eric</creatorcontrib><creatorcontrib>Kaffke, Anna</creatorcontrib><creatorcontrib>Bennstein, Sabrina B.</creatorcontrib><creatorcontrib>Koyro, Tobias</creatorcontrib><creatorcontrib>Peters, Anett</creatorcontrib><creatorcontrib>Velden, Joachim</creatorcontrib><creatorcontrib>Hünemörder, Stefanie</creatorcontrib><creatorcontrib>Haag, Friedrich</creatorcontrib><creatorcontrib>Steinmetz, Oliver M.</creatorcontrib><creatorcontrib>Mittrücker, Hans‐Willi</creatorcontrib><creatorcontrib>Stahl, Rolf A. K.</creatorcontrib><creatorcontrib>Panzer, Ulf</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schmidt, Tilman</au><au>Paust, Hans‐Joachim</au><au>Krebs, Christian F.</au><au>Turner, Jan‐Eric</au><au>Kaffke, Anna</au><au>Bennstein, Sabrina B.</au><au>Koyro, Tobias</au><au>Peters, Anett</au><au>Velden, Joachim</au><au>Hünemörder, Stefanie</au><au>Haag, Friedrich</au><au>Steinmetz, Oliver M.</au><au>Mittrücker, Hans‐Willi</au><au>Stahl, Rolf A. K.</au><au>Panzer, Ulf</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheumatol</addtitle><date>2015-02</date><risdate>2015</risdate><volume>67</volume><issue>2</issue><spage>475</spage><epage>487</epage><pages>475-487</pages><issn>2326-5191</issn><eissn>2326-5205</eissn><abstract>Objective
The CD4+ T cell immune response plays a pivotal role in the immunopathogenesis of human and experimental lupus nephritis, but the contribution of the Th17/interleukin‐17 (IL‐17) immune pathway to renal tissue injury in systemic lupus erythematosus (SLE) remains to be elucidated. The aim of this study was to characterize the function of the Th17/IL‐17A immune response in 2 murine models of lupus nephritis.
Methods
IL‐17A–deficient MRL/MPJ‐Faslpr/2J (MRL/lpr) mice were generated, and the clinical course of nephritis was monitored by assessing the levels of albuminuria, extent of renal tissue injury, and functional parameters. In addition, lupus‐prone (NZB × NZW)F1 (NZB/NZW) mice were treated with anti–IL‐17A and anti–interferon‐γ (anti‐IFNγ) antibodies, and their effects on the clinical course of lupus nephritis were assessed.
Results
Characterization of renal IL‐17A–producing and IFNγ‐producing T cells in MRL/lpr and NZB/NZW mice revealed low numbers of infiltrating CD3+IL‐17A+ cells. Renal IL‐17A was mainly produced by CD4/CD8 double‐negative CD3+ T cells and CD4+ Th17 cells. In contrast, the number of renal CD3+IFNγ+ cells continuously increased over time and largely consisted of typical CD4+ Th1 cells. IL‐17A deficiency did not affect the morphologic or functional parameters in MRL/lpr mice with lupus nephritis, nor did IL‐17A neutralization affect the clinical course of nephritis in NZB/NZW mice, but anti‐IFNγ treatment attenuated the severity of the disease.
Conclusion
The Th17/IL‐17A immune response plays no major role in the immunopathogenesis of lupus nephritis in MRL/lpr and NZB/NZW mice. Thus, the results of this study do not support the hypothesis that IL‐17A targeting could be an intriguing new therapeutic approach for the management of proliferative lupus nephritis in SLE patients.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>25385550</pmid><doi>10.1002/art.38955</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2326-5191 |
| ispartof | Arthritis & rheumatology (Hoboken, N.J.), 2015-02, Vol.67 (2), p.475-487 |
| issn | 2326-5191 2326-5205 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1660429600 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Alma/SFX Local Collection |
| subjects | Animals Antibodies, Anti-Idiotypic - pharmacology CD3 Complex - metabolism Disease Models, Animal Female Immunity, Cellular - immunology Immunity, Cellular - physiology Interferon-gamma - antagonists & inhibitors Interferon-gamma - immunology Interferon-gamma - physiology Interleukin-17 - antagonists & inhibitors Interleukin-17 - immunology Interleukin-17 - physiology Lupus Nephritis - immunology Lupus Nephritis - pathology Lupus Nephritis - physiopathology Male Mice Mice, Inbred MRL lpr Mice, Inbred NZB Mice, Knockout Severity of Illness Index T-Lymphocytes - pathology T-Lymphocytes - physiology Th17 Cells - pathology Th17 Cells - physiology |
| title | Function of the Th17/Interleukin‐17A Immune Response in Murine Lupus Nephritis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T05%3A20%3A09IST&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=Function%20of%20the%20Th17/Interleukin%E2%80%9017A%20Immune%20Response%20in%20Murine%20Lupus%20Nephritis&rft.jtitle=Arthritis%20&%20rheumatology%20(Hoboken,%20N.J.)&rft.au=Schmidt,%20Tilman&rft.date=2015-02&rft.volume=67&rft.issue=2&rft.spage=475&rft.epage=487&rft.pages=475-487&rft.issn=2326-5191&rft.eissn=2326-5205&rft_id=info:doi/10.1002/art.38955&rft_dat=%3Cproquest_cross%3E3571032751%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=1648595470&rft_id=info:pmid/25385550&rfr_iscdi=true |