A possible role for TSLP in inflammatory arthritis
Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that triggers dendritic cell-mediated Th2-type inflammatory responses and is considered as a master switch for allergic inflammation. In this study, we found increased levels of TSLP and, also TNF-α as previously reported, in synovial flui...
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Veröffentlicht in: | Biochemical and biophysical research communications 2007-05, Vol.357 (1), p.99-104 |
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creator | Koyama, Kensuke Ozawa, Tetsuro Hatsushika, Kyosuke Ando, Takashi Takano, Shinichi Wako, Masanori Suenaga, Fumiko Ohnuma, Yuko Ohba, Tetsuro Katoh, Ryohei Sugiyama, Hajime Hamada, Yoshiki Ogawa, Hideoki Okumura, Ko Nakao, Atsuhito |
description | Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that triggers dendritic cell-mediated Th2-type inflammatory responses and is considered as a master switch for allergic inflammation. In this study, we found increased levels of TSLP and, also TNF-α as previously reported, in synovial fluid specimens derived from patients with rheumatoid arthritis (RA) when compared with those from patients with osteoarthritis (OA). In addition, TNF-α up-regulated TSLP expression in RA- and OA-derived synovial fibroblasts, which was inhibited by IFN-γ. Furthermore, anti-TSLP neutralizing antibody ameliorated a TNF-α-dependent experimental arthritis induced by anti-type II collagen antibody in mice. Collectively, these results suggest that TSLP, as a downstream molecule of TNF-α, may be involved in the pathophysiology of inflammatory arthritis. TSLP might thus play a role not only in allergic diseases but also in inflammatory arthritis such as RA. |
doi_str_mv | 10.1016/j.bbrc.2007.03.081 |
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In this study, we found increased levels of TSLP and, also TNF-α as previously reported, in synovial fluid specimens derived from patients with rheumatoid arthritis (RA) when compared with those from patients with osteoarthritis (OA). In addition, TNF-α up-regulated TSLP expression in RA- and OA-derived synovial fibroblasts, which was inhibited by IFN-γ. Furthermore, anti-TSLP neutralizing antibody ameliorated a TNF-α-dependent experimental arthritis induced by anti-type II collagen antibody in mice. Collectively, these results suggest that TSLP, as a downstream molecule of TNF-α, may be involved in the pathophysiology of inflammatory arthritis. TSLP might thus play a role not only in allergic diseases but also in inflammatory arthritis such as RA.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2007.03.081</identifier><identifier>PMID: 17416344</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Arthritis, Rheumatoid - immunology ; Cells, Cultured ; Cytokines - immunology ; Female ; Fibroblasts - drug effects ; Fibroblasts - immunology ; Humans ; Male ; Middle Aged ; Osteoarthritis - immunology ; Rheumatoid arthritis ; Synovial fibroblasts ; Synovial Fluid - drug effects ; Synovial Fluid - immunology ; TNF-α ; TSLP ; Tumor Necrosis Factor-alpha - administration & dosage ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>Biochemical and biophysical research communications, 2007-05, Vol.357 (1), p.99-104</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-dcfefdeecc15d5909024128d1d19bb23a3675c486aad6d3864d436fad9030e633</citedby><cites>FETCH-LOGICAL-c385t-dcfefdeecc15d5909024128d1d19bb23a3675c486aad6d3864d436fad9030e633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X07005694$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17416344$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Koyama, Kensuke</creatorcontrib><creatorcontrib>Ozawa, Tetsuro</creatorcontrib><creatorcontrib>Hatsushika, Kyosuke</creatorcontrib><creatorcontrib>Ando, Takashi</creatorcontrib><creatorcontrib>Takano, Shinichi</creatorcontrib><creatorcontrib>Wako, Masanori</creatorcontrib><creatorcontrib>Suenaga, Fumiko</creatorcontrib><creatorcontrib>Ohnuma, Yuko</creatorcontrib><creatorcontrib>Ohba, Tetsuro</creatorcontrib><creatorcontrib>Katoh, Ryohei</creatorcontrib><creatorcontrib>Sugiyama, Hajime</creatorcontrib><creatorcontrib>Hamada, Yoshiki</creatorcontrib><creatorcontrib>Ogawa, Hideoki</creatorcontrib><creatorcontrib>Okumura, Ko</creatorcontrib><creatorcontrib>Nakao, Atsuhito</creatorcontrib><title>A possible role for TSLP in inflammatory arthritis</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that triggers dendritic cell-mediated Th2-type inflammatory responses and is considered as a master switch for allergic inflammation. In this study, we found increased levels of TSLP and, also TNF-α as previously reported, in synovial fluid specimens derived from patients with rheumatoid arthritis (RA) when compared with those from patients with osteoarthritis (OA). In addition, TNF-α up-regulated TSLP expression in RA- and OA-derived synovial fibroblasts, which was inhibited by IFN-γ. Furthermore, anti-TSLP neutralizing antibody ameliorated a TNF-α-dependent experimental arthritis induced by anti-type II collagen antibody in mice. Collectively, these results suggest that TSLP, as a downstream molecule of TNF-α, may be involved in the pathophysiology of inflammatory arthritis. TSLP might thus play a role not only in allergic diseases but also in inflammatory arthritis such as RA.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Cells, Cultured</subject><subject>Cytokines - immunology</subject><subject>Female</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - immunology</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Osteoarthritis - immunology</subject><subject>Rheumatoid arthritis</subject><subject>Synovial fibroblasts</subject><subject>Synovial Fluid - drug effects</subject><subject>Synovial Fluid - immunology</subject><subject>TNF-α</subject><subject>TSLP</subject><subject>Tumor Necrosis Factor-alpha - administration & dosage</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1Lw0AQhhdRbK3-AQ-Sk7fE2Y9sEvBSxC8oKFjB27LZneCWpKm7qdB_74YWvCkMM5dnXmYeQi4pZBSovFllde1NxgCKDHgGJT0iUwoVpIyCOCZTAJApq-jHhJyFsAKgVMjqlExoIajkQkwJmyebPgRXt5j4Pram98nybfGauHWsptVdp4fe7xLth0_vBhfOyUmj24AXhzkj7w_3y7undPHy-Hw3X6SGl_mQWtNgYxGNobnNq3gWE5SVllpa1TXjmssiN6KUWltpeSmFFVw22lbAASXnM3K9z934_muLYVCdCwbbVq-x3wZVgADG8-pfkAGTpahGkO1B4-PPHhu18a7TfqcoqFGpWqlRqRqVKuAqKo1LV4f0bd2h_V05OIzA7R7AKOPboVfBOFwbtM6jGZTt3V_5P7dPhjg</recordid><startdate>20070525</startdate><enddate>20070525</enddate><creator>Koyama, Kensuke</creator><creator>Ozawa, Tetsuro</creator><creator>Hatsushika, Kyosuke</creator><creator>Ando, Takashi</creator><creator>Takano, Shinichi</creator><creator>Wako, Masanori</creator><creator>Suenaga, Fumiko</creator><creator>Ohnuma, Yuko</creator><creator>Ohba, Tetsuro</creator><creator>Katoh, Ryohei</creator><creator>Sugiyama, Hajime</creator><creator>Hamada, Yoshiki</creator><creator>Ogawa, Hideoki</creator><creator>Okumura, Ko</creator><creator>Nakao, Atsuhito</creator><general>Elsevier 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>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20070525</creationdate><title>A possible role for TSLP in inflammatory arthritis</title><author>Koyama, Kensuke ; Ozawa, Tetsuro ; Hatsushika, Kyosuke ; Ando, Takashi ; Takano, Shinichi ; Wako, Masanori ; Suenaga, Fumiko ; Ohnuma, Yuko ; Ohba, Tetsuro ; Katoh, Ryohei ; Sugiyama, Hajime ; Hamada, Yoshiki ; Ogawa, Hideoki ; Okumura, Ko ; Nakao, Atsuhito</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-dcfefdeecc15d5909024128d1d19bb23a3675c486aad6d3864d436fad9030e633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Cells, Cultured</topic><topic>Cytokines - immunology</topic><topic>Female</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - immunology</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Osteoarthritis - immunology</topic><topic>Rheumatoid arthritis</topic><topic>Synovial fibroblasts</topic><topic>Synovial Fluid - drug effects</topic><topic>Synovial Fluid - immunology</topic><topic>TNF-α</topic><topic>TSLP</topic><topic>Tumor Necrosis Factor-alpha - administration & dosage</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Koyama, Kensuke</creatorcontrib><creatorcontrib>Ozawa, Tetsuro</creatorcontrib><creatorcontrib>Hatsushika, Kyosuke</creatorcontrib><creatorcontrib>Ando, Takashi</creatorcontrib><creatorcontrib>Takano, Shinichi</creatorcontrib><creatorcontrib>Wako, Masanori</creatorcontrib><creatorcontrib>Suenaga, Fumiko</creatorcontrib><creatorcontrib>Ohnuma, Yuko</creatorcontrib><creatorcontrib>Ohba, Tetsuro</creatorcontrib><creatorcontrib>Katoh, Ryohei</creatorcontrib><creatorcontrib>Sugiyama, Hajime</creatorcontrib><creatorcontrib>Hamada, Yoshiki</creatorcontrib><creatorcontrib>Ogawa, Hideoki</creatorcontrib><creatorcontrib>Okumura, Ko</creatorcontrib><creatorcontrib>Nakao, Atsuhito</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koyama, Kensuke</au><au>Ozawa, Tetsuro</au><au>Hatsushika, Kyosuke</au><au>Ando, Takashi</au><au>Takano, Shinichi</au><au>Wako, Masanori</au><au>Suenaga, Fumiko</au><au>Ohnuma, Yuko</au><au>Ohba, Tetsuro</au><au>Katoh, Ryohei</au><au>Sugiyama, Hajime</au><au>Hamada, Yoshiki</au><au>Ogawa, Hideoki</au><au>Okumura, Ko</au><au>Nakao, Atsuhito</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A possible role for TSLP in inflammatory arthritis</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2007-05-25</date><risdate>2007</risdate><volume>357</volume><issue>1</issue><spage>99</spage><epage>104</epage><pages>99-104</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Thymic stromal lymphopoietin (TSLP) is an IL-7-like cytokine that triggers dendritic cell-mediated Th2-type inflammatory responses and is considered as a master switch for allergic inflammation. In this study, we found increased levels of TSLP and, also TNF-α as previously reported, in synovial fluid specimens derived from patients with rheumatoid arthritis (RA) when compared with those from patients with osteoarthritis (OA). In addition, TNF-α up-regulated TSLP expression in RA- and OA-derived synovial fibroblasts, which was inhibited by IFN-γ. Furthermore, anti-TSLP neutralizing antibody ameliorated a TNF-α-dependent experimental arthritis induced by anti-type II collagen antibody in mice. Collectively, these results suggest that TSLP, as a downstream molecule of TNF-α, may be involved in the pathophysiology of inflammatory arthritis. TSLP might thus play a role not only in allergic diseases but also in inflammatory arthritis such as RA.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17416344</pmid><doi>10.1016/j.bbrc.2007.03.081</doi><tpages>6</tpages></addata></record> |
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subjects | Adult Aged Aged, 80 and over Arthritis, Rheumatoid - immunology Cells, Cultured Cytokines - immunology Female Fibroblasts - drug effects Fibroblasts - immunology Humans Male Middle Aged Osteoarthritis - immunology Rheumatoid arthritis Synovial fibroblasts Synovial Fluid - drug effects Synovial Fluid - immunology TNF-α TSLP Tumor Necrosis Factor-alpha - administration & dosage Tumor Necrosis Factor-alpha - immunology |
title | A possible role for TSLP in inflammatory arthritis |
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