Functional genomics identifies type I interferon pathway as central for host defense against Candida albicans

Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. Here by integrating transcriptional analysis and functional genomics, we identified Candida -specific host defence mechanisms in humans. Candi...

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Veröffentlicht in:	Nature communications 2013-01, Vol.4 (1), p.1342-1342, Article 1342
Hauptverfasser:	Smeekens, Sanne P., Ng, Aylwin, Kumar, Vinod, Johnson, Melissa D., Plantinga, Theo S., van Diemen, Cleo, Arts, Peer, Verwiel, Eugène T. P., Gresnigt, Mark S., Fransen, Karin, van Sommeren, Suzanne, Oosting, Marije, Cheng, Shih-Chin, Joosten, Leo A. B., Hoischen, Alexander, Kullberg, Bart-Jan, Scott, William K., Perfect, John R., van der Meer, Jos W. M., Wijmenga, Cisca, Netea, Mihai G., Xavier, Ramnik J.
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Sprache:	eng
Schlagworte:	631/208/191 631/250/127/1212 631/250/516 631/326/193/2544 alpha -Interferon Candida albicans Candida albicans - immunology Candidemia - genetics Candidemia - immunology Candidemia - microbiology Candidiasis Candidiasis, Chronic Mucocutaneous - genetics Candidiasis, Chronic Mucocutaneous - immunology Candidiasis, Chronic Mucocutaneous - microbiology Case-Control Studies Chronic mucocutaneous candidiasis Cluster Analysis Defense Disseminated infection Gene Expression Regulation Gene polymorphism Genes Genetic Predisposition to Disease Genetics Genomics Helper cells Host-Pathogen Interactions - genetics Host-Pathogen Interactions - immunology Humanities and Social Sciences Humans Immunity Immunotherapy Infections Inflammation Interferon Interferon Type I - genetics Interferon Type I - immunology Lymphocytes T Mucosa multidisciplinary Mutation - genetics Pathogens Peripheral blood mononuclear cells Polymorphism, Single Nucleotide - genetics Science Science (multidisciplinary) Signal Transduction - genetics Signal Transduction - immunology STAT1 Transcription Factor - genetics Th1 Cells - immunology Th17 Cells - immunology Transcription Transcription, Genetic
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creator	Smeekens, Sanne P. Ng, Aylwin Kumar, Vinod Johnson, Melissa D. Plantinga, Theo S. van Diemen, Cleo Arts, Peer Verwiel, Eugène T. P. Gresnigt, Mark S. Fransen, Karin van Sommeren, Suzanne Oosting, Marije Cheng, Shih-Chin Joosten, Leo A. B. Hoischen, Alexander Kullberg, Bart-Jan Scott, William K. Perfect, John R. van der Meer, Jos W. M. Wijmenga, Cisca Netea, Mihai G. Xavier, Ramnik J.
description	Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. Here by integrating transcriptional analysis and functional genomics, we identified Candida -specific host defence mechanisms in humans. Candida induced significant expression of genes from the type I interferon pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I interferon pathway in anti- Candida host defence was supported by additional evidence. Polymorphisms in type I interferon genes modulated Candida -induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in vitro experiments, type I interferons skewed Candida -induced inflammation from a Th17 response towards a Th1 response. Patients with chronic mucocutaneous candidiasis displayed defective expression of genes in the type I interferon pathway. These findings indicate that the type I interferon pathway is a main signature of Candida -induced inflammation and has a crucial role in anti- Candida host defence in humans. Systemic infection with the fungal pathogen C. albicans is characterized by high mortality, and the precise antifungal defence mechanisms in humans are poorly defined. Using a systems approach, Smeekens et al . describe a previously unknown role for type I interferons in human anti- Candida defence.
doi_str_mv	10.1038/ncomms2343
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Here by integrating transcriptional analysis and functional genomics, we identified Candida -specific host defence mechanisms in humans. Candida induced significant expression of genes from the type I interferon pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I interferon pathway in anti- Candida host defence was supported by additional evidence. Polymorphisms in type I interferon genes modulated Candida -induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in vitro experiments, type I interferons skewed Candida -induced inflammation from a Th17 response towards a Th1 response. Patients with chronic mucocutaneous candidiasis displayed defective expression of genes in the type I interferon pathway. These findings indicate that the type I interferon pathway is a main signature of Candida -induced inflammation and has a crucial role in anti- Candida host defence in humans. Systemic infection with the fungal pathogen C. albicans is characterized by high mortality, and the precise antifungal defence mechanisms in humans are poorly defined. 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M.</creatorcontrib><creatorcontrib>Wijmenga, Cisca</creatorcontrib><creatorcontrib>Netea, Mihai G.</creatorcontrib><creatorcontrib>Xavier, Ramnik J.</creatorcontrib><title>Functional genomics identifies type I interferon pathway as central for host defense against Candida albicans</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. Here by integrating transcriptional analysis and functional genomics, we identified Candida -specific host defence mechanisms in humans. Candida induced significant expression of genes from the type I interferon pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I interferon pathway in anti- Candida host defence was supported by additional evidence. Polymorphisms in type I interferon genes modulated Candida -induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in vitro experiments, type I interferons skewed Candida -induced inflammation from a Th17 response towards a Th1 response. Patients with chronic mucocutaneous candidiasis displayed defective expression of genes in the type I interferon pathway. These findings indicate that the type I interferon pathway is a main signature of Candida -induced inflammation and has a crucial role in anti- Candida host defence in humans. Systemic infection with the fungal pathogen C. albicans is characterized by high mortality, and the precise antifungal defence mechanisms in humans are poorly defined. Using a systems approach, Smeekens et al . describe a previously unknown role for type I interferons in human anti- Candida defence.</description><subject>631/208/191</subject><subject>631/250/127/1212</subject><subject>631/250/516</subject><subject>631/326/193/2544</subject><subject>alpha -Interferon</subject><subject>Candida albicans</subject><subject>Candida albicans - immunology</subject><subject>Candidemia - genetics</subject><subject>Candidemia - immunology</subject><subject>Candidemia - microbiology</subject><subject>Candidiasis</subject><subject>Candidiasis, Chronic Mucocutaneous - genetics</subject><subject>Candidiasis, Chronic Mucocutaneous - immunology</subject><subject>Candidiasis, Chronic Mucocutaneous - microbiology</subject><subject>Case-Control Studies</subject><subject>Chronic mucocutaneous candidiasis</subject><subject>Cluster Analysis</subject><subject>Defense</subject><subject>Disseminated infection</subject><subject>Gene Expression Regulation</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genomics</subject><subject>Helper cells</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Host-Pathogen Interactions - immunology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Immunity</subject><subject>Immunotherapy</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interferon</subject><subject>Interferon Type I - genetics</subject><subject>Interferon Type I - immunology</subject><subject>Lymphocytes T</subject><subject>Mucosa</subject><subject>multidisciplinary</subject><subject>Mutation - genetics</subject><subject>Pathogens</subject><subject>Peripheral blood mononuclear cells</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>STAT1 Transcription Factor - genetics</subject><subject>Th1 Cells - immunology</subject><subject>Th17 Cells - immunology</subject><subject>Transcription</subject><subject>Transcription, Genetic</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU1LHDEYx4NYVKyXfgAJ9CItq3mdZC6FslQrCF7sOWTyshuZSbbJjGW_fbPsqmt7MJckPL_n_7z8AfiE0SVGVF5Fk4ahEMroATghiOEZFoQe7r2PwVkpj6ge2mLJ2BE4JpS0rWzJCRiup2jGkKLu4cLFNARTYLAujsEHV-C4Xjl4C0McXfYupwhXelz-0WuoCzQVyzXRpwyXqYzQOu9icVAvdIj1P9fRBquh7rtgdCwfwQev--LOdvcp-HX942H-c3Z3f3M7_343M0zwcSYkssxiIqmw3qPWEi4727oOSWk7oZHEXmCqMRZcIkOEoawVjTREI8wopafg21Z3NXWDs7s-1SqHQee1Sjqot5EYlmqRnhRtCKeCV4GLnUBOvydXRjWEYlzf6-jSVBSmmDeo4Qy9jxJBKWsYair6-R_0MU25rn5DScJ5nWFDfdlSJqdSsvMvfWOkNp6rV88rfL4_6Qv67HAFvm6BUkNx4fJezf_l_gK_Qbdx</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>Smeekens, Sanne P.</creator><creator>Ng, Aylwin</creator><creator>Kumar, Vinod</creator><creator>Johnson, Melissa D.</creator><creator>Plantinga, Theo S.</creator><creator>van Diemen, Cleo</creator><creator>Arts, Peer</creator><creator>Verwiel, Eugène T. 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M.</creatorcontrib><creatorcontrib>Wijmenga, Cisca</creatorcontrib><creatorcontrib>Netea, Mihai G.</creatorcontrib><creatorcontrib>Xavier, Ramnik J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Environment Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Smeekens, Sanne P.</au><au>Ng, Aylwin</au><au>Kumar, Vinod</au><au>Johnson, Melissa D.</au><au>Plantinga, Theo S.</au><au>van Diemen, Cleo</au><au>Arts, Peer</au><au>Verwiel, Eugène T. P.</au><au>Gresnigt, Mark S.</au><au>Fransen, Karin</au><au>van Sommeren, Suzanne</au><au>Oosting, Marije</au><au>Cheng, Shih-Chin</au><au>Joosten, Leo A. B.</au><au>Hoischen, Alexander</au><au>Kullberg, Bart-Jan</au><au>Scott, William K.</au><au>Perfect, John R.</au><au>van der Meer, Jos W. M.</au><au>Wijmenga, Cisca</au><au>Netea, Mihai G.</au><au>Xavier, Ramnik J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional genomics identifies type I interferon pathway as central for host defense against Candida albicans</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>4</volume><issue>1</issue><spage>1342</spage><epage>1342</epage><pages>1342-1342</pages><artnum>1342</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. Here by integrating transcriptional analysis and functional genomics, we identified Candida -specific host defence mechanisms in humans. Candida induced significant expression of genes from the type I interferon pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I interferon pathway in anti- Candida host defence was supported by additional evidence. Polymorphisms in type I interferon genes modulated Candida -induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in vitro experiments, type I interferons skewed Candida -induced inflammation from a Th17 response towards a Th1 response. Patients with chronic mucocutaneous candidiasis displayed defective expression of genes in the type I interferon pathway. These findings indicate that the type I interferon pathway is a main signature of Candida -induced inflammation and has a crucial role in anti- Candida host defence in humans. Systemic infection with the fungal pathogen C. albicans is characterized by high mortality, and the precise antifungal defence mechanisms in humans are poorly defined. Using a systems approach, Smeekens et al . describe a previously unknown role for type I interferons in human anti- Candida defence.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23299892</pmid><doi>10.1038/ncomms2343</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
fulltext	fulltext_linktorsrc
identifier	ISSN: 2041-1723
ispartof	Nature communications, 2013-01, Vol.4 (1), p.1342-1342, Article 1342
issn	2041-1723 2041-1723
language	eng
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source	Springer_OA刊
subjects	631/208/191 631/250/127/1212 631/250/516 631/326/193/2544 alpha -Interferon Candida albicans Candida albicans - immunology Candidemia - genetics Candidemia - immunology Candidemia - microbiology Candidiasis Candidiasis, Chronic Mucocutaneous - genetics Candidiasis, Chronic Mucocutaneous - immunology Candidiasis, Chronic Mucocutaneous - microbiology Case-Control Studies Chronic mucocutaneous candidiasis Cluster Analysis Defense Disseminated infection Gene Expression Regulation Gene polymorphism Genes Genetic Predisposition to Disease Genetics Genomics Helper cells Host-Pathogen Interactions - genetics Host-Pathogen Interactions - immunology Humanities and Social Sciences Humans Immunity Immunotherapy Infections Inflammation Interferon Interferon Type I - genetics Interferon Type I - immunology Lymphocytes T Mucosa multidisciplinary Mutation - genetics Pathogens Peripheral blood mononuclear cells Polymorphism, Single Nucleotide - genetics Science Science (multidisciplinary) Signal Transduction - genetics Signal Transduction - immunology STAT1 Transcription Factor - genetics Th1 Cells - immunology Th17 Cells - immunology Transcription Transcription, Genetic
title	Functional genomics identifies type I interferon pathway as central for host defense against Candida albicans
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