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CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines
Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA). In a mouse model of collagen-induced arthritis (CIA), we identified and pur...
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Published in: | Arthritis research & therapy 2019-08, Vol.21 (1), p.198-198, Article 198 |
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creator | Takaki-Kuwahara, Ayako Arinobu, Yojiro Miyawaki, Kohta Yamada, Hisakata Tsuzuki, Hirofumi Irino, Kensuke Ayano, Masahiro Kimoto, Yasutaka Mitoma, Hiroki Akahoshi, Mitsuteru Tsukamoto, Hiroshi Horiuchi, Takahiko Niiro, Hiroaki Akashi, Koichi |
description | Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA).
In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients.
In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p |
doi_str_mv | 10.1186/s13075-019-1984-x |
format | article |
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In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients.
In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p < 0.0001 and p = 0.015). In RA patients, the proportion of CCR6+ ILCs in SF was positively correlated with tender joint counts (TJC) and swollen joint counts (SJC) (ρ=0.689, p = 0.0032 and ρ=0.644, p = 0.0071, respectively). Levels of CC chemokine ligand 20 (CCL20) increased in SF of patients with RA and were significantly correlated with CCR6+ ILC number (ρ=0.697, p = 0.0001).
CCR6+ ILC3s may play some roles in the development of RA through the production of IL-17 and IL-22.</description><identifier>ISSN: 1478-6362</identifier><identifier>ISSN: 1478-6354</identifier><identifier>EISSN: 1478-6362</identifier><identifier>DOI: 10.1186/s13075-019-1984-x</identifier><identifier>PMID: 31470891</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Anopheles ; Arthritis ; Care and treatment ; CCR6 ; Cells (Biology) ; Cellular biology ; Collagen ; Cytokines ; Diagnosis ; Fluorescence ; Inflammation ; Innate lymphoid cells ; Laboratory rats ; Lymphoid tissue ; Medical research ; Messenger RNA ; Polymerase chain reaction ; Rheumatoid arthritis ; Rheumatoid factor ; RNA ; Rodents ; Th17 cytokines</subject><ispartof>Arthritis research & therapy, 2019-08, Vol.21 (1), p.198-198, Article 198</ispartof><rights>COPYRIGHT 2019 BioMed Central Ltd.</rights><rights>2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c710t-68bbb655e7a1eaa4361dbc121df224a59f5e82faf4a570c025b7fd02c72ee2163</citedby><cites>FETCH-LOGICAL-c710t-68bbb655e7a1eaa4361dbc121df224a59f5e82faf4a570c025b7fd02c72ee2163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6716915/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2292826136?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,36992,44569,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31470891$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takaki-Kuwahara, Ayako</creatorcontrib><creatorcontrib>Arinobu, Yojiro</creatorcontrib><creatorcontrib>Miyawaki, Kohta</creatorcontrib><creatorcontrib>Yamada, Hisakata</creatorcontrib><creatorcontrib>Tsuzuki, Hirofumi</creatorcontrib><creatorcontrib>Irino, Kensuke</creatorcontrib><creatorcontrib>Ayano, Masahiro</creatorcontrib><creatorcontrib>Kimoto, Yasutaka</creatorcontrib><creatorcontrib>Mitoma, Hiroki</creatorcontrib><creatorcontrib>Akahoshi, Mitsuteru</creatorcontrib><creatorcontrib>Tsukamoto, Hiroshi</creatorcontrib><creatorcontrib>Horiuchi, Takahiko</creatorcontrib><creatorcontrib>Niiro, Hiroaki</creatorcontrib><creatorcontrib>Akashi, Koichi</creatorcontrib><title>CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines</title><title>Arthritis research & therapy</title><addtitle>Arthritis Res Ther</addtitle><description>Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA).
In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients.
In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p < 0.0001 and p = 0.015). In RA patients, the proportion of CCR6+ ILCs in SF was positively correlated with tender joint counts (TJC) and swollen joint counts (SJC) (ρ=0.689, p = 0.0032 and ρ=0.644, p = 0.0071, respectively). Levels of CC chemokine ligand 20 (CCL20) increased in SF of patients with RA and were significantly correlated with CCR6+ ILC number (ρ=0.697, p = 0.0001).
CCR6+ ILC3s may play some roles in the development of RA through the production of IL-17 and IL-22.</description><subject>Anopheles</subject><subject>Arthritis</subject><subject>Care and treatment</subject><subject>CCR6</subject><subject>Cells (Biology)</subject><subject>Cellular biology</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>Diagnosis</subject><subject>Fluorescence</subject><subject>Inflammation</subject><subject>Innate lymphoid cells</subject><subject>Laboratory rats</subject><subject>Lymphoid tissue</subject><subject>Medical research</subject><subject>Messenger RNA</subject><subject>Polymerase chain reaction</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatoid factor</subject><subject>RNA</subject><subject>Rodents</subject><subject>Th17 cytokines</subject><issn>1478-6362</issn><issn>1478-6354</issn><issn>1478-6362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptklFr1TAUx4sobk4_gC8S8EUYnTlJm7Qvwrg4HQwEmc8hTZPbXNvkmqSy--1N7Zy7Ig00nHP-v-Sc_IviNeALgIa9j0Axr0sMbQltU5V3T4pTqHhTMsrI00f7k-JFjDuMCWlJ9bw4oTmDmxZOi7TZfGXnaBv8vEcUWedk0mg8TPvB2x4pPY4RSaXmaR6XjHV5mVFOukc7b12KSygMep5kWhQypCHYZLPK9WgffD8rjW4H4Egdkv9unY4vi2dGjlG_uv-fFd-uPt5uPpc3Xz5dby5vSsUBp5I1XdexutZcgpayogz6TgGB3hBSybo1tW6IkSbvOVaY1B03PSaKE60JMHpWXK_c3sud2Ac7yXAQXlrxO-DDVuTrWjVqUXWmwazqakZoxTOXc43zmFqMJeOGZ9aHlbWfu9y80i4FOR5BjzPODmLrfwrGgbVQZ8C7e0DwP2Ydk5hsXOYrnfZzFIQ0FHALFc2lb_8p3fk5uDwqsbxgQxhQ9rdqK3MD-VV8PlctUHHJcDYFW1kX_6nKX68nq7zTxub4kQBWgQo-xqDNQ4-AxWI7sdpOZIFYbCfusubN4-E8KP74jP4C6p3R4w</recordid><startdate>20190830</startdate><enddate>20190830</enddate><creator>Takaki-Kuwahara, Ayako</creator><creator>Arinobu, Yojiro</creator><creator>Miyawaki, Kohta</creator><creator>Yamada, Hisakata</creator><creator>Tsuzuki, Hirofumi</creator><creator>Irino, Kensuke</creator><creator>Ayano, Masahiro</creator><creator>Kimoto, Yasutaka</creator><creator>Mitoma, Hiroki</creator><creator>Akahoshi, Mitsuteru</creator><creator>Tsukamoto, Hiroshi</creator><creator>Horiuchi, Takahiko</creator><creator>Niiro, Hiroaki</creator><creator>Akashi, Koichi</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20190830</creationdate><title>CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines</title><author>Takaki-Kuwahara, Ayako ; Arinobu, Yojiro ; Miyawaki, Kohta ; Yamada, Hisakata ; Tsuzuki, Hirofumi ; Irino, Kensuke ; Ayano, Masahiro ; Kimoto, Yasutaka ; Mitoma, Hiroki ; Akahoshi, Mitsuteru ; Tsukamoto, Hiroshi ; Horiuchi, Takahiko ; Niiro, Hiroaki ; Akashi, Koichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c710t-68bbb655e7a1eaa4361dbc121df224a59f5e82faf4a570c025b7fd02c72ee2163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Anopheles</topic><topic>Arthritis</topic><topic>Care and treatment</topic><topic>CCR6</topic><topic>Cells (Biology)</topic><topic>Cellular biology</topic><topic>Collagen</topic><topic>Cytokines</topic><topic>Diagnosis</topic><topic>Fluorescence</topic><topic>Inflammation</topic><topic>Innate lymphoid cells</topic><topic>Laboratory rats</topic><topic>Lymphoid tissue</topic><topic>Medical research</topic><topic>Messenger RNA</topic><topic>Polymerase chain reaction</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatoid factor</topic><topic>RNA</topic><topic>Rodents</topic><topic>Th17 cytokines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takaki-Kuwahara, Ayako</creatorcontrib><creatorcontrib>Arinobu, Yojiro</creatorcontrib><creatorcontrib>Miyawaki, Kohta</creatorcontrib><creatorcontrib>Yamada, Hisakata</creatorcontrib><creatorcontrib>Tsuzuki, Hirofumi</creatorcontrib><creatorcontrib>Irino, Kensuke</creatorcontrib><creatorcontrib>Ayano, Masahiro</creatorcontrib><creatorcontrib>Kimoto, Yasutaka</creatorcontrib><creatorcontrib>Mitoma, Hiroki</creatorcontrib><creatorcontrib>Akahoshi, Mitsuteru</creatorcontrib><creatorcontrib>Tsukamoto, Hiroshi</creatorcontrib><creatorcontrib>Horiuchi, Takahiko</creatorcontrib><creatorcontrib>Niiro, Hiroaki</creatorcontrib><creatorcontrib>Akashi, Koichi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Arthritis research & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takaki-Kuwahara, Ayako</au><au>Arinobu, Yojiro</au><au>Miyawaki, Kohta</au><au>Yamada, Hisakata</au><au>Tsuzuki, Hirofumi</au><au>Irino, Kensuke</au><au>Ayano, Masahiro</au><au>Kimoto, Yasutaka</au><au>Mitoma, Hiroki</au><au>Akahoshi, Mitsuteru</au><au>Tsukamoto, Hiroshi</au><au>Horiuchi, Takahiko</au><au>Niiro, Hiroaki</au><au>Akashi, Koichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines</atitle><jtitle>Arthritis research & therapy</jtitle><addtitle>Arthritis Res Ther</addtitle><date>2019-08-30</date><risdate>2019</risdate><volume>21</volume><issue>1</issue><spage>198</spage><epage>198</epage><pages>198-198</pages><artnum>198</artnum><issn>1478-6362</issn><issn>1478-6354</issn><eissn>1478-6362</eissn><abstract>Recent studies show that innate lymphoid cells (ILCs) contribute to the development of chronic inflammation and autoimmune disease. In this study, we assessed the ILC function in the development of rheumatoid arthritis (RA).
In a mouse model of collagen-induced arthritis (CIA), we identified and purified the ILC subsets in peripheral blood (PB), local lymph nodes (LNs), and joints by fluorescence-activated cell sorting and used quantitative PCR to assess the expression levels of representative cytokines. We also correlated the frequencies of each ILC subset in synovial fluid (SF) with clinical parameters in RA patients.
In the CIA model, the proportion of CCR6+ ILC3s to total ILCs in joints with active inflammation significantly increased relative to non-arthritic joints (median 29.6% vs 16.7%, p = 0.035). CCR6+ ILC3s from mice with arthritis expressed significantly higher levels of IL-17A and IL-22 mRNA than did comparable cells from control mice (p < 0.0001 and p = 0.015). In RA patients, the proportion of CCR6+ ILCs in SF was positively correlated with tender joint counts (TJC) and swollen joint counts (SJC) (ρ=0.689, p = 0.0032 and ρ=0.644, p = 0.0071, respectively). Levels of CC chemokine ligand 20 (CCL20) increased in SF of patients with RA and were significantly correlated with CCR6+ ILC number (ρ=0.697, p = 0.0001).
CCR6+ ILC3s may play some roles in the development of RA through the production of IL-17 and IL-22.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>31470891</pmid><doi>10.1186/s13075-019-1984-x</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anopheles Arthritis Care and treatment CCR6 Cells (Biology) Cellular biology Collagen Cytokines Diagnosis Fluorescence Inflammation Innate lymphoid cells Laboratory rats Lymphoid tissue Medical research Messenger RNA Polymerase chain reaction Rheumatoid arthritis Rheumatoid factor RNA Rodents Th17 cytokines |
title | CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines |
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