Cytokine balance in kidney tissue from lupus nephritis patients
Objective. To identify the balance of Th1/Th2 cytokine expression in the kidney and evaluate the difference in cytokine balance between patients with lupus nephritis WHO classes IV and V. Methods. The expression of the CD40 molecule on cultured human mesangial cells was assessed by flow cytometry af...
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| Veröffentlicht in: | British journal of rheumatology 2003-08, Vol.42 (8), p.935-938 |
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| container_title | British journal of rheumatology |
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| creator | Uhm, W.‐S. Na, K. Song, G.‐W. Jung, S.‐S. Lee, T. Park, M.‐H. Yoo, D.‐H. |
| description | Objective. To identify the balance of Th1/Th2 cytokine expression in the kidney and evaluate the difference in cytokine balance between patients with lupus nephritis WHO classes IV and V. Methods. The expression of the CD40 molecule on cultured human mesangial cells was assessed by flow cytometry after stimulation with interferon γ (IFN‐γ) or other cytokines. Frozen sections of kidney tissue from 10 patients with lupus nephritis and two non‐SLE patients (with minimal‐change disease) were stained with monoclonal antibodies for interleukin (IL)‐4, IL‐10, IL‐12, IFN‐γ, CD4, CD8, CD40, CD68 and CD40L. Results. CD40 expression of cultured mesangial cells was up‐regulated by IFN‐γ, but was not down‐regulated in the presence of the Th2 cytokines IL‐4 and IL‐10. In the glomeruli, CD40 expression and the ratios of IFN‐γ‐/IL‐10‐, IL‐12‐/IL‐4‐ and (IFN‐γ+IL‐12)/(IL‐4+IL‐10)‐positive cells were significantly higher in class IV than in class V lupus nephritis (P < 0.05). Also CD40, IFN‐γ and the activity index derived from the renal biopsy were closely correlated. Conclusion. IFN‐γ may contribute to the pathogenesis of proliferative glomerulonephritis by the up‐regulation of CD40 and the activation of the cellular immune response in human lupus. |
| doi_str_mv | 10.1093/rheumatology/keg255 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_73487314</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20579889</sourcerecordid><originalsourceid>FETCH-LOGICAL-c472t-2e04e55f1abe05f4ca302c5c0c82a15b09f39dd052827706938580f4a31fa1073</originalsourceid><addsrcrecordid>eNqF0VtrFDEUB_AgFlurn0CQQdC3aU9uk-RJyqK2sMXFC4ovIZs9adOdm8kMuN_eyC6t-OJTQvI7h-T8CXlB4YyC4efpFufOTUM73OzOt3jDpHxETqhoWA2cs8f3eyaOydOc7wBAUq6fkGPKFAcJ7IS8XeymYRt7rNaudb3HKvbVNm563FVTzHnGKqShq9p5nHPV43ibYjmvRjdF7Kf8jBwF12Z8flhPydf3774sLuvlxw9Xi4tl7YViU80QBEoZqFsjyCC848C89OA1c1SuwQRuNhuQTDOloDFcSw1BOE6Do6D4KXmz7zum4eeMebJdzB7b8mYc5mwVF1pxKv4LGUhltDYFvvoH3g1z6ssnLDWyaWSjm4L4Hvk05Jww2DHFzqWdpWD_pGD_TsHuUyhVLw-t53WHm4eaw9gLeH0ALnvXhlQmH_ODE0YLw3Rx9d7FPOGv-3uXtrZRXEl7-f2HXZlPq9X18rP9xn8DnmSi7g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>195665686</pqid></control><display><type>article</type><title>Cytokine balance in kidney tissue from lupus nephritis patients</title><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Alma/SFX Local Collection</source><creator>Uhm, W.‐S. ; Na, K. ; Song, G.‐W. ; Jung, S.‐S. ; Lee, T. ; Park, M.‐H. ; Yoo, D.‐H.</creator><creatorcontrib>Uhm, W.‐S. ; Na, K. ; Song, G.‐W. ; Jung, S.‐S. ; Lee, T. ; Park, M.‐H. ; Yoo, D.‐H.</creatorcontrib><description>Objective. To identify the balance of Th1/Th2 cytokine expression in the kidney and evaluate the difference in cytokine balance between patients with lupus nephritis WHO classes IV and V. Methods. The expression of the CD40 molecule on cultured human mesangial cells was assessed by flow cytometry after stimulation with interferon γ (IFN‐γ) or other cytokines. Frozen sections of kidney tissue from 10 patients with lupus nephritis and two non‐SLE patients (with minimal‐change disease) were stained with monoclonal antibodies for interleukin (IL)‐4, IL‐10, IL‐12, IFN‐γ, CD4, CD8, CD40, CD68 and CD40L. Results. CD40 expression of cultured mesangial cells was up‐regulated by IFN‐γ, but was not down‐regulated in the presence of the Th2 cytokines IL‐4 and IL‐10. In the glomeruli, CD40 expression and the ratios of IFN‐γ‐/IL‐10‐, IL‐12‐/IL‐4‐ and (IFN‐γ+IL‐12)/(IL‐4+IL‐10)‐positive cells were significantly higher in class IV than in class V lupus nephritis (P < 0.05). Also CD40, IFN‐γ and the activity index derived from the renal biopsy were closely correlated. Conclusion. IFN‐γ may contribute to the pathogenesis of proliferative glomerulonephritis by the up‐regulation of CD40 and the activation of the cellular immune response in human lupus.</description><identifier>ISSN: 1462-0324</identifier><identifier>ISSN: 1460-2172</identifier><identifier>EISSN: 1462-0332</identifier><identifier>EISSN: 1460-2172</identifier><identifier>DOI: 10.1093/rheumatology/keg255</identifier><identifier>PMID: 12730502</identifier><identifier>CODEN: BJRHDF</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Acute Disease ; Biological and medical sciences ; Case-Control Studies ; CD40 ; CD40 Antigens - analysis ; Cytokine ; Cytokines - analysis ; Humans ; Immunohistochemistry - methods ; Interferon-gamma - analysis ; Interferon‐γ ; Interleukin-10 - analysis ; Interleukin-4 - analysis ; Kidney Glomerulus - immunology ; Lupus nephritis ; Lupus Nephritis - immunology ; Medical sciences ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Statistics, Nonparametric ; Systemic lupus erythematosus ; Th1 Cells - immunology ; Th2 Cells - immunology</subject><ispartof>British journal of rheumatology, 2003-08, Vol.42 (8), p.935-938</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Aug 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-2e04e55f1abe05f4ca302c5c0c82a15b09f39dd052827706938580f4a31fa1073</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=14984928$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12730502$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uhm, W.‐S.</creatorcontrib><creatorcontrib>Na, K.</creatorcontrib><creatorcontrib>Song, G.‐W.</creatorcontrib><creatorcontrib>Jung, S.‐S.</creatorcontrib><creatorcontrib>Lee, T.</creatorcontrib><creatorcontrib>Park, M.‐H.</creatorcontrib><creatorcontrib>Yoo, D.‐H.</creatorcontrib><title>Cytokine balance in kidney tissue from lupus nephritis patients</title><title>British journal of rheumatology</title><addtitle>Rheumatology</addtitle><description>Objective. To identify the balance of Th1/Th2 cytokine expression in the kidney and evaluate the difference in cytokine balance between patients with lupus nephritis WHO classes IV and V. Methods. The expression of the CD40 molecule on cultured human mesangial cells was assessed by flow cytometry after stimulation with interferon γ (IFN‐γ) or other cytokines. Frozen sections of kidney tissue from 10 patients with lupus nephritis and two non‐SLE patients (with minimal‐change disease) were stained with monoclonal antibodies for interleukin (IL)‐4, IL‐10, IL‐12, IFN‐γ, CD4, CD8, CD40, CD68 and CD40L. Results. CD40 expression of cultured mesangial cells was up‐regulated by IFN‐γ, but was not down‐regulated in the presence of the Th2 cytokines IL‐4 and IL‐10. In the glomeruli, CD40 expression and the ratios of IFN‐γ‐/IL‐10‐, IL‐12‐/IL‐4‐ and (IFN‐γ+IL‐12)/(IL‐4+IL‐10)‐positive cells were significantly higher in class IV than in class V lupus nephritis (P < 0.05). Also CD40, IFN‐γ and the activity index derived from the renal biopsy were closely correlated. Conclusion. IFN‐γ may contribute to the pathogenesis of proliferative glomerulonephritis by the up‐regulation of CD40 and the activation of the cellular immune response in human lupus.</description><subject>Acute Disease</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>CD40</subject><subject>CD40 Antigens - analysis</subject><subject>Cytokine</subject><subject>Cytokines - analysis</subject><subject>Humans</subject><subject>Immunohistochemistry - methods</subject><subject>Interferon-gamma - analysis</subject><subject>Interferon‐γ</subject><subject>Interleukin-10 - analysis</subject><subject>Interleukin-4 - analysis</subject><subject>Kidney Glomerulus - immunology</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - immunology</subject><subject>Medical sciences</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Statistics, Nonparametric</subject><subject>Systemic lupus erythematosus</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - immunology</subject><issn>1462-0324</issn><issn>1460-2172</issn><issn>1462-0332</issn><issn>1460-2172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0VtrFDEUB_AgFlurn0CQQdC3aU9uk-RJyqK2sMXFC4ovIZs9adOdm8kMuN_eyC6t-OJTQvI7h-T8CXlB4YyC4efpFufOTUM73OzOt3jDpHxETqhoWA2cs8f3eyaOydOc7wBAUq6fkGPKFAcJ7IS8XeymYRt7rNaudb3HKvbVNm563FVTzHnGKqShq9p5nHPV43ibYjmvRjdF7Kf8jBwF12Z8flhPydf3774sLuvlxw9Xi4tl7YViU80QBEoZqFsjyCC848C89OA1c1SuwQRuNhuQTDOloDFcSw1BOE6Do6D4KXmz7zum4eeMebJdzB7b8mYc5mwVF1pxKv4LGUhltDYFvvoH3g1z6ssnLDWyaWSjm4L4Hvk05Jww2DHFzqWdpWD_pGD_TsHuUyhVLw-t53WHm4eaw9gLeH0ALnvXhlQmH_ODE0YLw3Rx9d7FPOGv-3uXtrZRXEl7-f2HXZlPq9X18rP9xn8DnmSi7g</recordid><startdate>20030801</startdate><enddate>20030801</enddate><creator>Uhm, W.‐S.</creator><creator>Na, K.</creator><creator>Song, G.‐W.</creator><creator>Jung, S.‐S.</creator><creator>Lee, T.</creator><creator>Park, M.‐H.</creator><creator>Yoo, D.‐H.</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>K9.</scope><scope>NAPCQ</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20030801</creationdate><title>Cytokine balance in kidney tissue from lupus nephritis patients</title><author>Uhm, W.‐S. ; Na, K. ; Song, G.‐W. ; Jung, S.‐S. ; Lee, T. ; Park, M.‐H. ; Yoo, D.‐H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-2e04e55f1abe05f4ca302c5c0c82a15b09f39dd052827706938580f4a31fa1073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acute Disease</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>CD40</topic><topic>CD40 Antigens - analysis</topic><topic>Cytokine</topic><topic>Cytokines - analysis</topic><topic>Humans</topic><topic>Immunohistochemistry - methods</topic><topic>Interferon-gamma - analysis</topic><topic>Interferon‐γ</topic><topic>Interleukin-10 - analysis</topic><topic>Interleukin-4 - analysis</topic><topic>Kidney Glomerulus - immunology</topic><topic>Lupus nephritis</topic><topic>Lupus Nephritis - immunology</topic><topic>Medical sciences</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Statistics, Nonparametric</topic><topic>Systemic lupus erythematosus</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uhm, W.‐S.</creatorcontrib><creatorcontrib>Na, K.</creatorcontrib><creatorcontrib>Song, G.‐W.</creatorcontrib><creatorcontrib>Jung, S.‐S.</creatorcontrib><creatorcontrib>Lee, T.</creatorcontrib><creatorcontrib>Park, M.‐H.</creatorcontrib><creatorcontrib>Yoo, D.‐H.</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uhm, W.‐S.</au><au>Na, K.</au><au>Song, G.‐W.</au><au>Jung, S.‐S.</au><au>Lee, T.</au><au>Park, M.‐H.</au><au>Yoo, D.‐H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytokine balance in kidney tissue from lupus nephritis patients</atitle><jtitle>British journal of rheumatology</jtitle><addtitle>Rheumatology</addtitle><date>2003-08-01</date><risdate>2003</risdate><volume>42</volume><issue>8</issue><spage>935</spage><epage>938</epage><pages>935-938</pages><issn>1462-0324</issn><issn>1460-2172</issn><eissn>1462-0332</eissn><eissn>1460-2172</eissn><coden>BJRHDF</coden><abstract>Objective. To identify the balance of Th1/Th2 cytokine expression in the kidney and evaluate the difference in cytokine balance between patients with lupus nephritis WHO classes IV and V. Methods. The expression of the CD40 molecule on cultured human mesangial cells was assessed by flow cytometry after stimulation with interferon γ (IFN‐γ) or other cytokines. Frozen sections of kidney tissue from 10 patients with lupus nephritis and two non‐SLE patients (with minimal‐change disease) were stained with monoclonal antibodies for interleukin (IL)‐4, IL‐10, IL‐12, IFN‐γ, CD4, CD8, CD40, CD68 and CD40L. Results. CD40 expression of cultured mesangial cells was up‐regulated by IFN‐γ, but was not down‐regulated in the presence of the Th2 cytokines IL‐4 and IL‐10. In the glomeruli, CD40 expression and the ratios of IFN‐γ‐/IL‐10‐, IL‐12‐/IL‐4‐ and (IFN‐γ+IL‐12)/(IL‐4+IL‐10)‐positive cells were significantly higher in class IV than in class V lupus nephritis (P < 0.05). Also CD40, IFN‐γ and the activity index derived from the renal biopsy were closely correlated. Conclusion. IFN‐γ may contribute to the pathogenesis of proliferative glomerulonephritis by the up‐regulation of CD40 and the activation of the cellular immune response in human lupus.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12730502</pmid><doi>10.1093/rheumatology/keg255</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Biological and medical sciences Case-Control Studies CD40 CD40 Antigens - analysis Cytokine Cytokines - analysis Humans Immunohistochemistry - methods Interferon-gamma - analysis Interferon‐γ Interleukin-10 - analysis Interleukin-4 - analysis Kidney Glomerulus - immunology Lupus nephritis Lupus Nephritis - immunology Medical sciences Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Statistics, Nonparametric Systemic lupus erythematosus Th1 Cells - immunology Th2 Cells - immunology |
| title | Cytokine balance in kidney tissue from lupus nephritis patients |
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