Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus
Objective Recently we serendipitously identified a patient with systemic lupus erythematosus (SLE) who was positive for autoantibodies to CD94/natural killer receptor group 2A (NKG2A). The present study was undertaken to investigate the occurrence and function of autoantibodies targeting lectin‐like...
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| Veröffentlicht in: | Arthritis & rheumatology (Hoboken, N.J.) N.J.), 2015-04, Vol.67 (4), p.1000-1011 |
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| creator | Hagberg, Niklas Theorell, Jakob Hjorton, Karin Spee, Pieter Eloranta, Maija‐Leena Bryceson, Yenan T. Rönnblom, Lars |
| description | Objective
Recently we serendipitously identified a patient with systemic lupus erythematosus (SLE) who was positive for autoantibodies to CD94/natural killer receptor group 2A (NKG2A). The present study was undertaken to investigate the occurrence and function of autoantibodies targeting lectin‐like NK cell receptors in SLE.
Methods
Sera from 203 SLE patients and 90 healthy individuals were analyzed, by flow cytometry, for Ig binding to Ba/F3 cells transfected with CD94/NKG2A, CD94/NKG2C, or NKG2D. Autoantibodies identified were characterized with regard to interference with HLA–E binding, effect on NK cell activation in response to HLA–E‐transfected K562 cells, and capacity to facilitate antibody‐dependent cell‐mediated cytotoxicity (ADCC). Levels of autoantibodies were determined in longitudinally sampled sera, and correlations with disease activity (SLE Disease Activity Index 2000) and severity (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) were investigated.
Results
Anti‐CD94/NKG2A autoantibodies were identified in 7 SLE patients. The autoantibodies from 6 patients inhibited binding of HLA–E to CD94/NKG2A, whereas those from the seventh patient augmented this binding. Autoantibodies from 2 patients also reacted with the activating receptor CD94/NKG2C, with inhibition of the binding of HLA–E to CD94/NKG2C observed in 1 case and enhancement of this binding in the other. None of the sera contained anti‐NKG2D autoantibodies. The levels of anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies correlated with disease activity and with a more severe SLE phenotype. Mechanistically, anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies both interfered with HLA–E‐mediated regulation of NK cell activation and facilitated the elimination of target cells expressing CD94/NKG2A or CD94/NKG2C through ADCC.
Conclusion
Anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies occur in a subset of patients with clinically active SLE. Given their capacity to deplete certain NK cell subsets and interfere with particular NK cell function, such autoantibodies may promote the pathogenesis of SLE. |
| doi_str_mv | 10.1002/art.38999 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_516845</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3636964321</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5039-becd5b1d0d4dd84415d2b3c8c2dd63f0f4cbf577685769aeefc39580a180da5b3</originalsourceid><addsrcrecordid>eNp1kstu1DAYhSMEolXpghdAkdiARDq-JvEyml6oOmoRFFhaju1QlyQefFE1Ox6BZ-RJ8DQzgwQab_zr6DvHlv6TZS8hOIEAoJlw4QTXjLEn2SHCqCwoAvTpdoYMHmTH3t-DdFgFSkCfZweIUggIJoeZPY-jDMaOos-bMZjfP3_NTxmZXV9doCYXo_pPnedNDFYktbXKaJ-bMf8ggtFj8PlXE-7yTysf9GBkvojL6PMztwp3ehDB-uhfZM860Xt9vLmPss_nZ7fz98Xi5uJy3iwKSQFmRauloi1UQBGlakIgVajFspZIqRJ3oCOy7WhVlTWtSia07iRmtAYC1kAJ2uKjrJhy_YNexpYvnRmEW3ErDN9I39OkOYVlTWji2V5-6az6a9oaIQYsPV5Xyftur_fUfGm4dd94jBylbVQk4W8mPOX-iNoHPhgvdd-LUdvoOSzLapf8-h_03kaXdvVIles0uKbeTpR01nunu90PIODrjvDUEf7YkcS-2iTGdtBqR24bkYDZBDyYXq_2J_Hm4-0U-Qcq3Meo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1666974317</pqid></control><display><type>article</type><title>Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><source>Alma/SFX Local Collection</source><creator>Hagberg, Niklas ; Theorell, Jakob ; Hjorton, Karin ; Spee, Pieter ; Eloranta, Maija‐Leena ; Bryceson, Yenan T. ; Rönnblom, Lars</creator><creatorcontrib>Hagberg, Niklas ; Theorell, Jakob ; Hjorton, Karin ; Spee, Pieter ; Eloranta, Maija‐Leena ; Bryceson, Yenan T. ; Rönnblom, Lars</creatorcontrib><description>Objective
Recently we serendipitously identified a patient with systemic lupus erythematosus (SLE) who was positive for autoantibodies to CD94/natural killer receptor group 2A (NKG2A). The present study was undertaken to investigate the occurrence and function of autoantibodies targeting lectin‐like NK cell receptors in SLE.
Methods
Sera from 203 SLE patients and 90 healthy individuals were analyzed, by flow cytometry, for Ig binding to Ba/F3 cells transfected with CD94/NKG2A, CD94/NKG2C, or NKG2D. Autoantibodies identified were characterized with regard to interference with HLA–E binding, effect on NK cell activation in response to HLA–E‐transfected K562 cells, and capacity to facilitate antibody‐dependent cell‐mediated cytotoxicity (ADCC). Levels of autoantibodies were determined in longitudinally sampled sera, and correlations with disease activity (SLE Disease Activity Index 2000) and severity (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) were investigated.
Results
Anti‐CD94/NKG2A autoantibodies were identified in 7 SLE patients. The autoantibodies from 6 patients inhibited binding of HLA–E to CD94/NKG2A, whereas those from the seventh patient augmented this binding. Autoantibodies from 2 patients also reacted with the activating receptor CD94/NKG2C, with inhibition of the binding of HLA–E to CD94/NKG2C observed in 1 case and enhancement of this binding in the other. None of the sera contained anti‐NKG2D autoantibodies. The levels of anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies correlated with disease activity and with a more severe SLE phenotype. Mechanistically, anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies both interfered with HLA–E‐mediated regulation of NK cell activation and facilitated the elimination of target cells expressing CD94/NKG2A or CD94/NKG2C through ADCC.
Conclusion
Anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies occur in a subset of patients with clinically active SLE. Given their capacity to deplete certain NK cell subsets and interfere with particular NK cell function, such autoantibodies may promote the pathogenesis of SLE.</description><identifier>ISSN: 2326-5191</identifier><identifier>ISSN: 2326-5205</identifier><identifier>EISSN: 2326-5205</identifier><identifier>DOI: 10.1002/art.38999</identifier><identifier>PMID: 25510434</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Autoantibodies - blood ; Autoimmune diseases ; Humans ; Immune system ; Lupus ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - immunology ; Lymphocyte Activation - immunology ; Medical Science ; Medicin och hälsovetenskap ; Medicinsk vetenskap ; NK Cell Lectin-Like Receptor Subfamily C - immunology ; NK Cell Lectin-Like Receptor Subfamily D - immunology ; Patients ; Studies</subject><ispartof>Arthritis & rheumatology (Hoboken, N.J.), 2015-04, Vol.67 (4), p.1000-1011</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-c5039-becd5b1d0d4dd84415d2b3c8c2dd63f0f4cbf577685769aeefc39580a180da5b3</citedby><cites>FETCH-LOGICAL-c5039-becd5b1d0d4dd84415d2b3c8c2dd63f0f4cbf577685769aeefc39580a180da5b3</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.38999$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fart.38999$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,782,786,887,1419,27933,27934,45583,45584</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25510434$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-251974$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:130957687$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Hagberg, Niklas</creatorcontrib><creatorcontrib>Theorell, Jakob</creatorcontrib><creatorcontrib>Hjorton, Karin</creatorcontrib><creatorcontrib>Spee, Pieter</creatorcontrib><creatorcontrib>Eloranta, Maija‐Leena</creatorcontrib><creatorcontrib>Bryceson, Yenan T.</creatorcontrib><creatorcontrib>Rönnblom, Lars</creatorcontrib><title>Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus</title><title>Arthritis & rheumatology (Hoboken, N.J.)</title><addtitle>Arthritis Rheumatol</addtitle><description>Objective
Recently we serendipitously identified a patient with systemic lupus erythematosus (SLE) who was positive for autoantibodies to CD94/natural killer receptor group 2A (NKG2A). The present study was undertaken to investigate the occurrence and function of autoantibodies targeting lectin‐like NK cell receptors in SLE.
Methods
Sera from 203 SLE patients and 90 healthy individuals were analyzed, by flow cytometry, for Ig binding to Ba/F3 cells transfected with CD94/NKG2A, CD94/NKG2C, or NKG2D. Autoantibodies identified were characterized with regard to interference with HLA–E binding, effect on NK cell activation in response to HLA–E‐transfected K562 cells, and capacity to facilitate antibody‐dependent cell‐mediated cytotoxicity (ADCC). Levels of autoantibodies were determined in longitudinally sampled sera, and correlations with disease activity (SLE Disease Activity Index 2000) and severity (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) were investigated.
Results
Anti‐CD94/NKG2A autoantibodies were identified in 7 SLE patients. The autoantibodies from 6 patients inhibited binding of HLA–E to CD94/NKG2A, whereas those from the seventh patient augmented this binding. Autoantibodies from 2 patients also reacted with the activating receptor CD94/NKG2C, with inhibition of the binding of HLA–E to CD94/NKG2C observed in 1 case and enhancement of this binding in the other. None of the sera contained anti‐NKG2D autoantibodies. The levels of anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies correlated with disease activity and with a more severe SLE phenotype. Mechanistically, anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies both interfered with HLA–E‐mediated regulation of NK cell activation and facilitated the elimination of target cells expressing CD94/NKG2A or CD94/NKG2C through ADCC.
Conclusion
Anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies occur in a subset of patients with clinically active SLE. Given their capacity to deplete certain NK cell subsets and interfere with particular NK cell function, such autoantibodies may promote the pathogenesis of SLE.</description><subject>Autoantibodies - blood</subject><subject>Autoimmune diseases</subject><subject>Humans</subject><subject>Immune system</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - blood</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lymphocyte Activation - immunology</subject><subject>Medical Science</subject><subject>Medicin och hälsovetenskap</subject><subject>Medicinsk vetenskap</subject><subject>NK Cell Lectin-Like Receptor Subfamily C - immunology</subject><subject>NK Cell Lectin-Like Receptor Subfamily D - immunology</subject><subject>Patients</subject><subject>Studies</subject><issn>2326-5191</issn><issn>2326-5205</issn><issn>2326-5205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kstu1DAYhSMEolXpghdAkdiARDq-JvEyml6oOmoRFFhaju1QlyQefFE1Ox6BZ-RJ8DQzgwQab_zr6DvHlv6TZS8hOIEAoJlw4QTXjLEn2SHCqCwoAvTpdoYMHmTH3t-DdFgFSkCfZweIUggIJoeZPY-jDMaOos-bMZjfP3_NTxmZXV9doCYXo_pPnedNDFYktbXKaJ-bMf8ggtFj8PlXE-7yTysf9GBkvojL6PMztwp3ehDB-uhfZM860Xt9vLmPss_nZ7fz98Xi5uJy3iwKSQFmRauloi1UQBGlakIgVajFspZIqRJ3oCOy7WhVlTWtSia07iRmtAYC1kAJ2uKjrJhy_YNexpYvnRmEW3ErDN9I39OkOYVlTWji2V5-6az6a9oaIQYsPV5Xyftur_fUfGm4dd94jBylbVQk4W8mPOX-iNoHPhgvdd-LUdvoOSzLapf8-h_03kaXdvVIles0uKbeTpR01nunu90PIODrjvDUEf7YkcS-2iTGdtBqR24bkYDZBDyYXq_2J_Hm4-0U-Qcq3Meo</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>Hagberg, Niklas</creator><creator>Theorell, Jakob</creator><creator>Hjorton, Karin</creator><creator>Spee, Pieter</creator><creator>Eloranta, Maija‐Leena</creator><creator>Bryceson, Yenan T.</creator><creator>Rönnblom, Lars</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><scope>ADTPV</scope><scope>AOWAS</scope><scope>DF2</scope></search><sort><creationdate>201504</creationdate><title>Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus</title><author>Hagberg, Niklas ; Theorell, Jakob ; Hjorton, Karin ; Spee, Pieter ; Eloranta, Maija‐Leena ; Bryceson, Yenan T. ; Rönnblom, Lars</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5039-becd5b1d0d4dd84415d2b3c8c2dd63f0f4cbf577685769aeefc39580a180da5b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Autoantibodies - blood</topic><topic>Autoimmune diseases</topic><topic>Humans</topic><topic>Immune system</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - blood</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lymphocyte Activation - immunology</topic><topic>Medical Science</topic><topic>Medicin och hälsovetenskap</topic><topic>Medicinsk vetenskap</topic><topic>NK Cell Lectin-Like Receptor Subfamily C - immunology</topic><topic>NK Cell Lectin-Like Receptor Subfamily D - immunology</topic><topic>Patients</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hagberg, Niklas</creatorcontrib><creatorcontrib>Theorell, Jakob</creatorcontrib><creatorcontrib>Hjorton, Karin</creatorcontrib><creatorcontrib>Spee, Pieter</creatorcontrib><creatorcontrib>Eloranta, Maija‐Leena</creatorcontrib><creatorcontrib>Bryceson, Yenan T.</creatorcontrib><creatorcontrib>Rönnblom, Lars</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><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Uppsala universitet</collection><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hagberg, Niklas</au><au>Theorell, Jakob</au><au>Hjorton, Karin</au><au>Spee, Pieter</au><au>Eloranta, Maija‐Leena</au><au>Bryceson, Yenan T.</au><au>Rönnblom, Lars</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus</atitle><jtitle>Arthritis & rheumatology (Hoboken, N.J.)</jtitle><addtitle>Arthritis Rheumatol</addtitle><date>2015-04</date><risdate>2015</risdate><volume>67</volume><issue>4</issue><spage>1000</spage><epage>1011</epage><pages>1000-1011</pages><issn>2326-5191</issn><issn>2326-5205</issn><eissn>2326-5205</eissn><abstract>Objective
Recently we serendipitously identified a patient with systemic lupus erythematosus (SLE) who was positive for autoantibodies to CD94/natural killer receptor group 2A (NKG2A). The present study was undertaken to investigate the occurrence and function of autoantibodies targeting lectin‐like NK cell receptors in SLE.
Methods
Sera from 203 SLE patients and 90 healthy individuals were analyzed, by flow cytometry, for Ig binding to Ba/F3 cells transfected with CD94/NKG2A, CD94/NKG2C, or NKG2D. Autoantibodies identified were characterized with regard to interference with HLA–E binding, effect on NK cell activation in response to HLA–E‐transfected K562 cells, and capacity to facilitate antibody‐dependent cell‐mediated cytotoxicity (ADCC). Levels of autoantibodies were determined in longitudinally sampled sera, and correlations with disease activity (SLE Disease Activity Index 2000) and severity (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index) were investigated.
Results
Anti‐CD94/NKG2A autoantibodies were identified in 7 SLE patients. The autoantibodies from 6 patients inhibited binding of HLA–E to CD94/NKG2A, whereas those from the seventh patient augmented this binding. Autoantibodies from 2 patients also reacted with the activating receptor CD94/NKG2C, with inhibition of the binding of HLA–E to CD94/NKG2C observed in 1 case and enhancement of this binding in the other. None of the sera contained anti‐NKG2D autoantibodies. The levels of anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies correlated with disease activity and with a more severe SLE phenotype. Mechanistically, anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies both interfered with HLA–E‐mediated regulation of NK cell activation and facilitated the elimination of target cells expressing CD94/NKG2A or CD94/NKG2C through ADCC.
Conclusion
Anti‐CD94/NKG2A and anti‐CD94/NKG2C autoantibodies occur in a subset of patients with clinically active SLE. Given their capacity to deplete certain NK cell subsets and interfere with particular NK cell function, such autoantibodies may promote the pathogenesis of SLE.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>25510434</pmid><doi>10.1002/art.38999</doi><tpages>12</tpages></addata></record> |
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| subjects | Autoantibodies - blood Autoimmune diseases Humans Immune system Lupus Lupus Erythematosus, Systemic - blood Lupus Erythematosus, Systemic - immunology Lymphocyte Activation - immunology Medical Science Medicin och hälsovetenskap Medicinsk vetenskap NK Cell Lectin-Like Receptor Subfamily C - immunology NK Cell Lectin-Like Receptor Subfamily D - immunology Patients Studies |
| title | Functional Anti‐CD94/NKG2A and Anti‐CD94/NKG2C Autoantibodies in Patients With Systemic Lupus Erythematosus |
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