Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs
In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D (PGD ) in the pathophysiology of SL...
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| Veröffentlicht in: | Nature communications 2018-02, Vol.9 (1), p.725 |
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| creator | Pellefigues, Christophe Dema, Barbara Lamri, Yasmine Saidoune, Fanny Chavarot, Nathalie Lohéac, Charlotte Pacreau, Emeline Dussiot, Michael Bidault, Caroline Marquet, Florian Jablonski, Mathieu Chemouny, Jonathan M Jouan, Fanny Dossier, Antoine Chauveheid, Marie-Paule Gobert, Delphine Papo, Thomas Karasuyama, Hajime Sacré, Karim Daugas, Eric Charles, Nicolas |
| description | In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D
(PGD
) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD
receptors (PTGDR) on blood basophils and increased concentration of PGD
metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD
induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD
can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD
/PTGDR axis as a ready-to-use therapeutic modality in SLE. |
| doi_str_mv | 10.1038/s41467-018-03129-8 |
| format | Article |
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(PGD
) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD
receptors (PTGDR) on blood basophils and increased concentration of PGD
metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD
induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD
can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD
/PTGDR axis as a ready-to-use therapeutic modality in SLE.</description><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-018-03129-8</identifier><identifier>PMID: 29463843</identifier><language>eng</language><publisher>England</publisher><subject>Adult ; Animals ; Basophils - immunology ; Female ; Humans ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - immunology ; Lymphatic System - immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Prostaglandin D2 - blood ; Prostaglandin D2 - immunology ; Receptors, CXCR4 - blood ; Receptors, CXCR4 - immunology ; Receptors, Immunologic - blood ; Receptors, Immunologic - immunology ; Receptors, Prostaglandin - blood ; Receptors, Prostaglandin - immunology ; Signal Transduction - immunology ; Young Adult</subject><ispartof>Nature communications, 2018-02, Vol.9 (1), p.725</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-6309-3986 ; 0000-0002-5416-5834</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29463843$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pellefigues, Christophe</creatorcontrib><creatorcontrib>Dema, Barbara</creatorcontrib><creatorcontrib>Lamri, Yasmine</creatorcontrib><creatorcontrib>Saidoune, Fanny</creatorcontrib><creatorcontrib>Chavarot, Nathalie</creatorcontrib><creatorcontrib>Lohéac, Charlotte</creatorcontrib><creatorcontrib>Pacreau, Emeline</creatorcontrib><creatorcontrib>Dussiot, Michael</creatorcontrib><creatorcontrib>Bidault, Caroline</creatorcontrib><creatorcontrib>Marquet, Florian</creatorcontrib><creatorcontrib>Jablonski, Mathieu</creatorcontrib><creatorcontrib>Chemouny, Jonathan M</creatorcontrib><creatorcontrib>Jouan, Fanny</creatorcontrib><creatorcontrib>Dossier, Antoine</creatorcontrib><creatorcontrib>Chauveheid, Marie-Paule</creatorcontrib><creatorcontrib>Gobert, Delphine</creatorcontrib><creatorcontrib>Papo, Thomas</creatorcontrib><creatorcontrib>Karasuyama, Hajime</creatorcontrib><creatorcontrib>Sacré, Karim</creatorcontrib><creatorcontrib>Daugas, Eric</creatorcontrib><creatorcontrib>Charles, Nicolas</creatorcontrib><title>Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><description>In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D
(PGD
) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD
receptors (PTGDR) on blood basophils and increased concentration of PGD
metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD
induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD
can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD
/PTGDR axis as a ready-to-use therapeutic modality in SLE.</description><subject>Adult</subject><subject>Animals</subject><subject>Basophils - immunology</subject><subject>Female</subject><subject>Humans</subject><subject>Lupus Erythematosus, Systemic - blood</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lymphatic System - immunology</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Middle Aged</subject><subject>Prostaglandin D2 - blood</subject><subject>Prostaglandin D2 - immunology</subject><subject>Receptors, CXCR4 - blood</subject><subject>Receptors, CXCR4 - immunology</subject><subject>Receptors, Immunologic - blood</subject><subject>Receptors, Immunologic - immunology</subject><subject>Receptors, Prostaglandin - blood</subject><subject>Receptors, Prostaglandin - immunology</subject><subject>Signal Transduction - immunology</subject><subject>Young Adult</subject><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjrtuAjEQRS2kCFDCD1Cg-QEnfgm8NQ-lTJEqzWpgza6RvbY864K_hyKpc5vTnCNdxtZSvEuh7QcZabY7LqTlQkvVcDtjSyWM5HKn9IKtiG7iOd1Ia8ycLVRjttoavWQ_XyXRhH3AsfMjHEABxhz81TuCUHMl6Dw5JAfTUFLtBzgjpTz4AHi51FgDTj6N8IzDPeYh-Q5S6XGkN_ZyxUBu9ctXtjkdv_efPNdzdF2bi49Y7u3fGf2v8AAEPEbD</recordid><startdate>20180220</startdate><enddate>20180220</enddate><creator>Pellefigues, Christophe</creator><creator>Dema, Barbara</creator><creator>Lamri, Yasmine</creator><creator>Saidoune, Fanny</creator><creator>Chavarot, Nathalie</creator><creator>Lohéac, Charlotte</creator><creator>Pacreau, Emeline</creator><creator>Dussiot, Michael</creator><creator>Bidault, Caroline</creator><creator>Marquet, Florian</creator><creator>Jablonski, Mathieu</creator><creator>Chemouny, Jonathan M</creator><creator>Jouan, Fanny</creator><creator>Dossier, Antoine</creator><creator>Chauveheid, Marie-Paule</creator><creator>Gobert, Delphine</creator><creator>Papo, Thomas</creator><creator>Karasuyama, Hajime</creator><creator>Sacré, Karim</creator><creator>Daugas, Eric</creator><creator>Charles, Nicolas</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><orcidid>https://orcid.org/0000-0001-6309-3986</orcidid><orcidid>https://orcid.org/0000-0002-5416-5834</orcidid></search><sort><creationdate>20180220</creationdate><title>Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs</title><author>Pellefigues, Christophe ; Dema, Barbara ; Lamri, Yasmine ; Saidoune, Fanny ; Chavarot, Nathalie ; Lohéac, Charlotte ; Pacreau, Emeline ; Dussiot, Michael ; Bidault, Caroline ; Marquet, Florian ; Jablonski, Mathieu ; Chemouny, Jonathan M ; Jouan, Fanny ; Dossier, Antoine ; Chauveheid, Marie-Paule ; Gobert, Delphine ; Papo, Thomas ; Karasuyama, Hajime ; Sacré, Karim ; Daugas, Eric ; Charles, Nicolas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_294638433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Basophils - immunology</topic><topic>Female</topic><topic>Humans</topic><topic>Lupus Erythematosus, Systemic - blood</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lymphatic System - immunology</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Middle Aged</topic><topic>Prostaglandin D2 - blood</topic><topic>Prostaglandin D2 - immunology</topic><topic>Receptors, CXCR4 - blood</topic><topic>Receptors, CXCR4 - immunology</topic><topic>Receptors, Immunologic - blood</topic><topic>Receptors, Immunologic - immunology</topic><topic>Receptors, Prostaglandin - blood</topic><topic>Receptors, Prostaglandin - immunology</topic><topic>Signal Transduction - immunology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pellefigues, Christophe</creatorcontrib><creatorcontrib>Dema, Barbara</creatorcontrib><creatorcontrib>Lamri, Yasmine</creatorcontrib><creatorcontrib>Saidoune, Fanny</creatorcontrib><creatorcontrib>Chavarot, Nathalie</creatorcontrib><creatorcontrib>Lohéac, Charlotte</creatorcontrib><creatorcontrib>Pacreau, Emeline</creatorcontrib><creatorcontrib>Dussiot, Michael</creatorcontrib><creatorcontrib>Bidault, Caroline</creatorcontrib><creatorcontrib>Marquet, Florian</creatorcontrib><creatorcontrib>Jablonski, Mathieu</creatorcontrib><creatorcontrib>Chemouny, Jonathan M</creatorcontrib><creatorcontrib>Jouan, Fanny</creatorcontrib><creatorcontrib>Dossier, Antoine</creatorcontrib><creatorcontrib>Chauveheid, Marie-Paule</creatorcontrib><creatorcontrib>Gobert, Delphine</creatorcontrib><creatorcontrib>Papo, Thomas</creatorcontrib><creatorcontrib>Karasuyama, Hajime</creatorcontrib><creatorcontrib>Sacré, Karim</creatorcontrib><creatorcontrib>Daugas, Eric</creatorcontrib><creatorcontrib>Charles, Nicolas</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pellefigues, Christophe</au><au>Dema, Barbara</au><au>Lamri, Yasmine</au><au>Saidoune, Fanny</au><au>Chavarot, Nathalie</au><au>Lohéac, Charlotte</au><au>Pacreau, Emeline</au><au>Dussiot, Michael</au><au>Bidault, Caroline</au><au>Marquet, Florian</au><au>Jablonski, Mathieu</au><au>Chemouny, Jonathan M</au><au>Jouan, Fanny</au><au>Dossier, Antoine</au><au>Chauveheid, Marie-Paule</au><au>Gobert, Delphine</au><au>Papo, Thomas</au><au>Karasuyama, Hajime</au><au>Sacré, Karim</au><au>Daugas, Eric</au><au>Charles, Nicolas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs</atitle><jtitle>Nature communications</jtitle><addtitle>Nat Commun</addtitle><date>2018-02-20</date><risdate>2018</risdate><volume>9</volume><issue>1</issue><spage>725</spage><pages>725-</pages><eissn>2041-1723</eissn><abstract>In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D
(PGD
) in the pathophysiology of SLE. Patients with SLE have increased expression of PGD
receptors (PTGDR) on blood basophils and increased concentration of PGD
metabolites in plasma. Through an autocrine mechanism dependent on both PTGDRs, PGD
induces the externalization of CXCR4 on basophils, both in humans and mice, driving accumulation in secondary lymphoid organs. Although PGD
can accelerate basophil-dependent disease, antagonizing PTGDRs in mice reduces lupus-like disease in spontaneous and induced mouse models. Our study identifies the PGD
/PTGDR axis as a ready-to-use therapeutic modality in SLE.</abstract><cop>England</cop><pmid>29463843</pmid><doi>10.1038/s41467-018-03129-8</doi><orcidid>https://orcid.org/0000-0001-6309-3986</orcidid><orcidid>https://orcid.org/0000-0002-5416-5834</orcidid></addata></record> |
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| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Springer Nature OA Free Journals |
| subjects | Adult Animals Basophils - immunology Female Humans Lupus Erythematosus, Systemic - blood Lupus Erythematosus, Systemic - immunology Lymphatic System - immunology Male Mice, Inbred C57BL Mice, Knockout Middle Aged Prostaglandin D2 - blood Prostaglandin D2 - immunology Receptors, CXCR4 - blood Receptors, CXCR4 - immunology Receptors, Immunologic - blood Receptors, Immunologic - immunology Receptors, Prostaglandin - blood Receptors, Prostaglandin - immunology Signal Transduction - immunology Young Adult |
| title | Prostaglandin D 2 amplifies lupus disease through basophil accumulation in lymphoid organs |
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