Expression of a pathogen-response program in peripheral blood cells defines a subgroup of Rheumatoid Arthritis patients
Rheumatoid arthritis (RA) is a heterogeneous disease with unknown etiology. Here we aimed to distinguish RA subtypes based on peripheral blood (PB) gene expression profiles in comparison with a pathogen-response transcriptional program. PB was obtained from 35 RA patients and 15 healthy individuals....
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| Veröffentlicht in: | Genes and immunity 2008-01, Vol.9 (1), p.16-22 |
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| creator | van der Pouw Kraan, T C T M van Baarsen, L G M Wijbrandts, C A Voskuyl, A E Rustenburg, F Baggen, J M Dijkmans, B A C Tak, P P Verweij, C L |
| description | Rheumatoid arthritis (RA) is a heterogeneous disease with unknown etiology. Here we aimed to distinguish RA subtypes based on peripheral blood (PB) gene expression profiles in comparison with a pathogen-response transcriptional program. PB was obtained from 35 RA patients and 15 healthy individuals. For expression profiling we used DNA microarrays. A combined cluster analysis of RA and control samples together with samples from a viral infection model revealed that the gene expression profile of a subgroup of RA patients (RA
A
) was reminiscent to that of poxvirus-infected macaques. Statistical analysis, followed by Gene Ontology analysis of the RA
A
patients confirmed that these patients form a distinct group, with activation of several host defense mechanisms that resemble a common host-pathogen response. Analysis of the promoter region of genes that were overexpressed in the RA
A
patients, revealed an enrichment of transcription factor binding sites for NFκB and interferon-activated transcription factors. Moreover, this subgroup of RA patients expressed significantly increased titers of anti-cyclic citrullinated peptide antibodies. We conclude that activation of a host-pathogen response defines a subgroup of RA patients characterized by increased autoreactivity against citrullinated proteins. |
| doi_str_mv | 10.1038/sj.gene.6364438 |
| format | Article |
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A
) was reminiscent to that of poxvirus-infected macaques. Statistical analysis, followed by Gene Ontology analysis of the RA
A
patients confirmed that these patients form a distinct group, with activation of several host defense mechanisms that resemble a common host-pathogen response. Analysis of the promoter region of genes that were overexpressed in the RA
A
patients, revealed an enrichment of transcription factor binding sites for NFκB and interferon-activated transcription factors. Moreover, this subgroup of RA patients expressed significantly increased titers of anti-cyclic citrullinated peptide antibodies. We conclude that activation of a host-pathogen response defines a subgroup of RA patients characterized by increased autoreactivity against citrullinated proteins.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6364438</identifier><identifier>PMID: 17928867</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Arthritis, Rheumatoid - blood ; Arthritis, Rheumatoid - classification ; Arthritis, Rheumatoid - genetics ; Binding sites ; Biomedical and Life Sciences ; Biomedicine ; Blood cells ; Cancer Research ; Case-Control Studies ; Citrulline ; Cluster Analysis ; Diagnosis ; DNA binding proteins ; DNA fingerprinting ; DNA microarrays ; Etiology ; Female ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Viral ; Genetic aspects ; Health aspects ; Host-Parasite Interactions ; Host-pathogen interactions ; Human Genetics ; Humans ; Immunology ; Interferon ; Leukocytes, Mononuclear - cytology ; Leukocytes, Mononuclear - metabolism ; Macaca ; Macaca - virology ; Male ; Middle Aged ; NF-κB protein ; Oligonucleotide Array Sequence Analysis ; original-article ; Pathogens ; Peripheral blood ; Physiological aspects ; Promoter Regions, Genetic ; Rheumatoid arthritis ; Risk factors ; Smallpox ; Statistical analysis ; Transcription factors ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Genes and immunity, 2008-01, Vol.9 (1), p.16-22</ispartof><rights>Springer Nature Limited 2008</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2008</rights><rights>Springer Nature Limited 2008.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c630t-98743156be1f16ce3ee15101be9625469cbba3fffcfa0eb9bfc1242f023b1ce13</citedby><cites>FETCH-LOGICAL-c630t-98743156be1f16ce3ee15101be9625469cbba3fffcfa0eb9bfc1242f023b1ce13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.gene.6364438$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6364438$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17928867$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Pouw Kraan, T C T M</creatorcontrib><creatorcontrib>van Baarsen, L G M</creatorcontrib><creatorcontrib>Wijbrandts, C A</creatorcontrib><creatorcontrib>Voskuyl, A E</creatorcontrib><creatorcontrib>Rustenburg, F</creatorcontrib><creatorcontrib>Baggen, J M</creatorcontrib><creatorcontrib>Dijkmans, B A C</creatorcontrib><creatorcontrib>Tak, P P</creatorcontrib><creatorcontrib>Verweij, C L</creatorcontrib><title>Expression of a pathogen-response program in peripheral blood cells defines a subgroup of Rheumatoid Arthritis patients</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Rheumatoid arthritis (RA) is a heterogeneous disease with unknown etiology. Here we aimed to distinguish RA subtypes based on peripheral blood (PB) gene expression profiles in comparison with a pathogen-response transcriptional program. PB was obtained from 35 RA patients and 15 healthy individuals. For expression profiling we used DNA microarrays. A combined cluster analysis of RA and control samples together with samples from a viral infection model revealed that the gene expression profile of a subgroup of RA patients (RA
A
) was reminiscent to that of poxvirus-infected macaques. Statistical analysis, followed by Gene Ontology analysis of the RA
A
patients confirmed that these patients form a distinct group, with activation of several host defense mechanisms that resemble a common host-pathogen response. Analysis of the promoter region of genes that were overexpressed in the RA
A
patients, revealed an enrichment of transcription factor binding sites for NFκB and interferon-activated transcription factors. Moreover, this subgroup of RA patients expressed significantly increased titers of anti-cyclic citrullinated peptide antibodies. We conclude that activation of a host-pathogen response defines a subgroup of RA patients characterized by increased autoreactivity against citrullinated proteins.</description><subject>Animals</subject><subject>Arthritis, Rheumatoid - blood</subject><subject>Arthritis, Rheumatoid - classification</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Binding sites</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood cells</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>Citrulline</subject><subject>Cluster Analysis</subject><subject>Diagnosis</subject><subject>DNA binding proteins</subject><subject>DNA fingerprinting</subject><subject>DNA microarrays</subject><subject>Etiology</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genes, Viral</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Host-Parasite Interactions</subject><subject>Host-pathogen interactions</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Interferon</subject><subject>Leukocytes, Mononuclear - cytology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Macaca</subject><subject>Macaca - virology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>NF-κB protein</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>original-article</subject><subject>Pathogens</subject><subject>Peripheral blood</subject><subject>Physiological aspects</subject><subject>Promoter Regions, Genetic</subject><subject>Rheumatoid arthritis</subject><subject>Risk factors</subject><subject>Smallpox</subject><subject>Statistical analysis</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFks-L1DAcxYso7rp69iZFQfDQ2fyaNDkOy6oLC8Kq55B2vulkaJOab4vrf2_KDKwjLpJDQvJ5L3nhFcVrSlaUcHWJ-1UHAVaSSyG4elKcU1HLai1q8nRZS1kJVeuz4gXinhAqqdTPizNaa6aUrM-Ln9f3YwJEH0MZXWnL0U67mD2rvDvGgFCOKXbJDqUP5QjJjztIti-bPsZt2ULfY7kF5wNgVuPcdCnO4-J1t4N5sFP023KTpl3yk8fF3kOY8GXxzNke4dVxvii-f7z-dvW5uv3y6eZqc1u1kpOp0qoWnK5lA9RR2QIHoGtKaANasrWQum0ay51zrbMEGt24ljLBHGG8oS1QflG8P_jmFD9mwMkMHpdX2wBxRlNnklNG_gsyoonUWmXw3V_gPs4p5BCGSUFrxongmXr7KEWV0rqmf1h1tgfjg4tTsu1yr9lQtWaa1UpkavUPKo8tDL6NIX9-3j8RfDgRZGaC-6mzM6K5-Xp3yl4e2DZFxATOjMkPNv0ylJilYgb3ZqmYOVYsK94ck83NANsH_tipDJADgPkodJAeoj_m-RsBdtzQ</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>van der Pouw Kraan, T C T M</creator><creator>van Baarsen, L G M</creator><creator>Wijbrandts, C A</creator><creator>Voskuyl, A E</creator><creator>Rustenburg, F</creator><creator>Baggen, J M</creator><creator>Dijkmans, B A C</creator><creator>Tak, P P</creator><creator>Verweij, C L</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7TM</scope><scope>7U9</scope><scope>7X8</scope></search><sort><creationdate>20080101</creationdate><title>Expression of a pathogen-response program in peripheral blood cells defines a subgroup of Rheumatoid Arthritis patients</title><author>van der Pouw Kraan, T C T M ; van Baarsen, L G M ; Wijbrandts, C A ; Voskuyl, A E ; Rustenburg, F ; Baggen, J M ; Dijkmans, B A C ; Tak, P P ; Verweij, C L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c630t-98743156be1f16ce3ee15101be9625469cbba3fffcfa0eb9bfc1242f023b1ce13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Arthritis, Rheumatoid - blood</topic><topic>Arthritis, Rheumatoid - classification</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Binding sites</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood cells</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Citrulline</topic><topic>Cluster Analysis</topic><topic>Diagnosis</topic><topic>DNA binding proteins</topic><topic>DNA fingerprinting</topic><topic>DNA microarrays</topic><topic>Etiology</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Genes, Viral</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Host-Parasite Interactions</topic><topic>Host-pathogen interactions</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Interferon</topic><topic>Leukocytes, Mononuclear - cytology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Macaca</topic><topic>Macaca - virology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>NF-κB protein</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>original-article</topic><topic>Pathogens</topic><topic>Peripheral blood</topic><topic>Physiological aspects</topic><topic>Promoter Regions, Genetic</topic><topic>Rheumatoid arthritis</topic><topic>Risk factors</topic><topic>Smallpox</topic><topic>Statistical analysis</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van der Pouw Kraan, T C T M</creatorcontrib><creatorcontrib>van Baarsen, L G M</creatorcontrib><creatorcontrib>Wijbrandts, C A</creatorcontrib><creatorcontrib>Voskuyl, A E</creatorcontrib><creatorcontrib>Rustenburg, F</creatorcontrib><creatorcontrib>Baggen, J M</creatorcontrib><creatorcontrib>Dijkmans, B A C</creatorcontrib><creatorcontrib>Tak, P P</creatorcontrib><creatorcontrib>Verweij, C L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Pouw Kraan, T C T M</au><au>van Baarsen, L G M</au><au>Wijbrandts, C A</au><au>Voskuyl, A E</au><au>Rustenburg, F</au><au>Baggen, J M</au><au>Dijkmans, B A C</au><au>Tak, P P</au><au>Verweij, C L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of a pathogen-response program in peripheral blood cells defines a subgroup of Rheumatoid Arthritis patients</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>9</volume><issue>1</issue><spage>16</spage><epage>22</epage><pages>16-22</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Rheumatoid arthritis (RA) is a heterogeneous disease with unknown etiology. Here we aimed to distinguish RA subtypes based on peripheral blood (PB) gene expression profiles in comparison with a pathogen-response transcriptional program. PB was obtained from 35 RA patients and 15 healthy individuals. For expression profiling we used DNA microarrays. A combined cluster analysis of RA and control samples together with samples from a viral infection model revealed that the gene expression profile of a subgroup of RA patients (RA
A
) was reminiscent to that of poxvirus-infected macaques. Statistical analysis, followed by Gene Ontology analysis of the RA
A
patients confirmed that these patients form a distinct group, with activation of several host defense mechanisms that resemble a common host-pathogen response. Analysis of the promoter region of genes that were overexpressed in the RA
A
patients, revealed an enrichment of transcription factor binding sites for NFκB and interferon-activated transcription factors. Moreover, this subgroup of RA patients expressed significantly increased titers of anti-cyclic citrullinated peptide antibodies. We conclude that activation of a host-pathogen response defines a subgroup of RA patients characterized by increased autoreactivity against citrullinated proteins.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17928867</pmid><doi>10.1038/sj.gene.6364438</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - classification Arthritis, Rheumatoid - genetics Binding sites Biomedical and Life Sciences Biomedicine Blood cells Cancer Research Case-Control Studies Citrulline Cluster Analysis Diagnosis DNA binding proteins DNA fingerprinting DNA microarrays Etiology Female Gene Expression Gene Expression Profiling Gene Expression Regulation Genes, Viral Genetic aspects Health aspects Host-Parasite Interactions Host-pathogen interactions Human Genetics Humans Immunology Interferon Leukocytes, Mononuclear - cytology Leukocytes, Mononuclear - metabolism Macaca Macaca - virology Male Middle Aged NF-κB protein Oligonucleotide Array Sequence Analysis original-article Pathogens Peripheral blood Physiological aspects Promoter Regions, Genetic Rheumatoid arthritis Risk factors Smallpox Statistical analysis Transcription factors Transcription Factors - genetics Transcription Factors - metabolism |
| title | Expression of a pathogen-response program in peripheral blood cells defines a subgroup of Rheumatoid Arthritis patients |
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