TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice

IL-1 receptor antagonist–deficient (IL-1Ra –/– ) mice spontaneously develop autoimmune arthritis. We demonstrate here that T cells are required for the induction of arthritis; T cell–deficient IL-1Ra –/– mice did not develop arthritis, and transfer of IL-1Ra –/– T cells induced arthritis in nu/nu mi...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of clinical investigation 2004-12, Vol.114 (11), p.1603-1611
Main Authors: Horai, Reiko, Nakajima, Akiko, Habiro, Katsuyoshi, Kotani, Motoko, Nakae, Susumu, Matsuki, Taizo, Nambu, Aya, Saijo, Shinobu, Kotaki, Hayato, Sudo, Katsuko, Okahara, Akihiko, Tanioka, Hidetoshi, Ikuse, Toshimi, Ishii, Naoto, Schwartzberg, Pamela L., Abe, Ryo, Iwakura, Yoichiro
Format: Article
Language:English
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 1611
container_issue 11
container_start_page 1603
container_title The Journal of clinical investigation
container_volume 114
creator Horai, Reiko
Nakajima, Akiko
Habiro, Katsuyoshi
Kotani, Motoko
Nakae, Susumu
Matsuki, Taizo
Nambu, Aya
Saijo, Shinobu
Kotaki, Hayato
Sudo, Katsuko
Okahara, Akihiko
Tanioka, Hidetoshi
Ikuse, Toshimi
Ishii, Naoto
Schwartzberg, Pamela L.
Abe, Ryo
Iwakura, Yoichiro
description IL-1 receptor antagonist–deficient (IL-1Ra –/– ) mice spontaneously develop autoimmune arthritis. We demonstrate here that T cells are required for the induction of arthritis; T cell–deficient IL-1Ra –/– mice did not develop arthritis, and transfer of IL-1Ra –/– T cells induced arthritis in nu/nu mice. Development of arthritis was also markedly suppressed by TNF-α deficiency. We found that TNF-α induced OX40 expression on T cells and blocking the interaction between either CD40 and its ligand or OX40 and its ligand suppressed development of arthritis. These findings suggest that IL-1 receptor antagonist deficiency in T cells disrupts homeostasis of the immune system and that TNF-α plays an important role in activating T cells through induction of OX40.
doi_str_mv 10.1172/JCI200420742
format article
fullrecord <record><control><sourceid>pubmedcentral</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_529278</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>pubmedcentral_primary_oai_pubmedcentral_nih_gov_529278</sourcerecordid><originalsourceid>FETCH-LOGICAL-p177t-82f62894d41f0215ae8bcda856470c0d70c146038c381ac25fd4385baf9e21f03</originalsourceid><addsrcrecordid>eNpVjjFOwzAYhT2AaClsHMAXCNiOXTsDA6ooLYpgKXPk2r9bV0kcOU4lNu7ASbgIh-AkBMHC8t7w9L33ELqi5JpSyW4eF2tGCGdEcnaCpoQwmhUyVxN03vcHQijngp-hCRVCKlKwKTpsnpbZ5wf2PTZxMF7X2IWI0x6whSPUoWugTTg4rIcUfNMMLWAd0z76NDK-xesyoziCgS6NoG6T3oXW9-nr7d2C88b_8I03cIFOna57uPzzGXpZ3m8Wq6x8flgv7sqso1KmTDE3Z6rgllM3_hca1NZYrcScS2KIHYXyOcmVyRXVhglnea7EVrsC2IjkM3T729sN2wasGfejrqsu-kbH1ypoX_1PWr-vduFYCVYwqfJvZLtmJg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice</title><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Horai, Reiko ; Nakajima, Akiko ; Habiro, Katsuyoshi ; Kotani, Motoko ; Nakae, Susumu ; Matsuki, Taizo ; Nambu, Aya ; Saijo, Shinobu ; Kotaki, Hayato ; Sudo, Katsuko ; Okahara, Akihiko ; Tanioka, Hidetoshi ; Ikuse, Toshimi ; Ishii, Naoto ; Schwartzberg, Pamela L. ; Abe, Ryo ; Iwakura, Yoichiro</creator><creatorcontrib>Horai, Reiko ; Nakajima, Akiko ; Habiro, Katsuyoshi ; Kotani, Motoko ; Nakae, Susumu ; Matsuki, Taizo ; Nambu, Aya ; Saijo, Shinobu ; Kotaki, Hayato ; Sudo, Katsuko ; Okahara, Akihiko ; Tanioka, Hidetoshi ; Ikuse, Toshimi ; Ishii, Naoto ; Schwartzberg, Pamela L. ; Abe, Ryo ; Iwakura, Yoichiro</creatorcontrib><description>IL-1 receptor antagonist–deficient (IL-1Ra –/– ) mice spontaneously develop autoimmune arthritis. We demonstrate here that T cells are required for the induction of arthritis; T cell–deficient IL-1Ra –/– mice did not develop arthritis, and transfer of IL-1Ra –/– T cells induced arthritis in nu/nu mice. Development of arthritis was also markedly suppressed by TNF-α deficiency. We found that TNF-α induced OX40 expression on T cells and blocking the interaction between either CD40 and its ligand or OX40 and its ligand suppressed development of arthritis. These findings suggest that IL-1 receptor antagonist deficiency in T cells disrupts homeostasis of the immune system and that TNF-α plays an important role in activating T cells through induction of OX40.</description><identifier>ISSN: 0021-9738</identifier><identifier>DOI: 10.1172/JCI200420742</identifier><identifier>PMID: 15578092</identifier><language>eng</language><publisher>American Society for Clinical Investigation</publisher><ispartof>The Journal of clinical investigation, 2004-12, Vol.114 (11), p.1603-1611</ispartof><rights>Copyright © 2004, American Society for Clinical Investigation 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC529278/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC529278/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>Horai, Reiko</creatorcontrib><creatorcontrib>Nakajima, Akiko</creatorcontrib><creatorcontrib>Habiro, Katsuyoshi</creatorcontrib><creatorcontrib>Kotani, Motoko</creatorcontrib><creatorcontrib>Nakae, Susumu</creatorcontrib><creatorcontrib>Matsuki, Taizo</creatorcontrib><creatorcontrib>Nambu, Aya</creatorcontrib><creatorcontrib>Saijo, Shinobu</creatorcontrib><creatorcontrib>Kotaki, Hayato</creatorcontrib><creatorcontrib>Sudo, Katsuko</creatorcontrib><creatorcontrib>Okahara, Akihiko</creatorcontrib><creatorcontrib>Tanioka, Hidetoshi</creatorcontrib><creatorcontrib>Ikuse, Toshimi</creatorcontrib><creatorcontrib>Ishii, Naoto</creatorcontrib><creatorcontrib>Schwartzberg, Pamela L.</creatorcontrib><creatorcontrib>Abe, Ryo</creatorcontrib><creatorcontrib>Iwakura, Yoichiro</creatorcontrib><title>TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice</title><title>The Journal of clinical investigation</title><description>IL-1 receptor antagonist–deficient (IL-1Ra –/– ) mice spontaneously develop autoimmune arthritis. We demonstrate here that T cells are required for the induction of arthritis; T cell–deficient IL-1Ra –/– mice did not develop arthritis, and transfer of IL-1Ra –/– T cells induced arthritis in nu/nu mice. Development of arthritis was also markedly suppressed by TNF-α deficiency. We found that TNF-α induced OX40 expression on T cells and blocking the interaction between either CD40 and its ligand or OX40 and its ligand suppressed development of arthritis. These findings suggest that IL-1 receptor antagonist deficiency in T cells disrupts homeostasis of the immune system and that TNF-α plays an important role in activating T cells through induction of OX40.</description><issn>0021-9738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpVjjFOwzAYhT2AaClsHMAXCNiOXTsDA6ooLYpgKXPk2r9bV0kcOU4lNu7ASbgIh-AkBMHC8t7w9L33ELqi5JpSyW4eF2tGCGdEcnaCpoQwmhUyVxN03vcHQijngp-hCRVCKlKwKTpsnpbZ5wf2PTZxMF7X2IWI0x6whSPUoWugTTg4rIcUfNMMLWAd0z76NDK-xesyoziCgS6NoG6T3oXW9-nr7d2C88b_8I03cIFOna57uPzzGXpZ3m8Wq6x8flgv7sqso1KmTDE3Z6rgllM3_hca1NZYrcScS2KIHYXyOcmVyRXVhglnea7EVrsC2IjkM3T729sN2wasGfejrqsu-kbH1ypoX_1PWr-vduFYCVYwqfJvZLtmJg</recordid><startdate>20041201</startdate><enddate>20041201</enddate><creator>Horai, Reiko</creator><creator>Nakajima, Akiko</creator><creator>Habiro, Katsuyoshi</creator><creator>Kotani, Motoko</creator><creator>Nakae, Susumu</creator><creator>Matsuki, Taizo</creator><creator>Nambu, Aya</creator><creator>Saijo, Shinobu</creator><creator>Kotaki, Hayato</creator><creator>Sudo, Katsuko</creator><creator>Okahara, Akihiko</creator><creator>Tanioka, Hidetoshi</creator><creator>Ikuse, Toshimi</creator><creator>Ishii, Naoto</creator><creator>Schwartzberg, Pamela L.</creator><creator>Abe, Ryo</creator><creator>Iwakura, Yoichiro</creator><general>American Society for Clinical Investigation</general><scope>5PM</scope></search><sort><creationdate>20041201</creationdate><title>TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice</title><author>Horai, Reiko ; Nakajima, Akiko ; Habiro, Katsuyoshi ; Kotani, Motoko ; Nakae, Susumu ; Matsuki, Taizo ; Nambu, Aya ; Saijo, Shinobu ; Kotaki, Hayato ; Sudo, Katsuko ; Okahara, Akihiko ; Tanioka, Hidetoshi ; Ikuse, Toshimi ; Ishii, Naoto ; Schwartzberg, Pamela L. ; Abe, Ryo ; Iwakura, Yoichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p177t-82f62894d41f0215ae8bcda856470c0d70c146038c381ac25fd4385baf9e21f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Horai, Reiko</creatorcontrib><creatorcontrib>Nakajima, Akiko</creatorcontrib><creatorcontrib>Habiro, Katsuyoshi</creatorcontrib><creatorcontrib>Kotani, Motoko</creatorcontrib><creatorcontrib>Nakae, Susumu</creatorcontrib><creatorcontrib>Matsuki, Taizo</creatorcontrib><creatorcontrib>Nambu, Aya</creatorcontrib><creatorcontrib>Saijo, Shinobu</creatorcontrib><creatorcontrib>Kotaki, Hayato</creatorcontrib><creatorcontrib>Sudo, Katsuko</creatorcontrib><creatorcontrib>Okahara, Akihiko</creatorcontrib><creatorcontrib>Tanioka, Hidetoshi</creatorcontrib><creatorcontrib>Ikuse, Toshimi</creatorcontrib><creatorcontrib>Ishii, Naoto</creatorcontrib><creatorcontrib>Schwartzberg, Pamela L.</creatorcontrib><creatorcontrib>Abe, Ryo</creatorcontrib><creatorcontrib>Iwakura, Yoichiro</creatorcontrib><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Horai, Reiko</au><au>Nakajima, Akiko</au><au>Habiro, Katsuyoshi</au><au>Kotani, Motoko</au><au>Nakae, Susumu</au><au>Matsuki, Taizo</au><au>Nambu, Aya</au><au>Saijo, Shinobu</au><au>Kotaki, Hayato</au><au>Sudo, Katsuko</au><au>Okahara, Akihiko</au><au>Tanioka, Hidetoshi</au><au>Ikuse, Toshimi</au><au>Ishii, Naoto</au><au>Schwartzberg, Pamela L.</au><au>Abe, Ryo</au><au>Iwakura, Yoichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice</atitle><jtitle>The Journal of clinical investigation</jtitle><date>2004-12-01</date><risdate>2004</risdate><volume>114</volume><issue>11</issue><spage>1603</spage><epage>1611</epage><pages>1603-1611</pages><issn>0021-9738</issn><abstract>IL-1 receptor antagonist–deficient (IL-1Ra –/– ) mice spontaneously develop autoimmune arthritis. We demonstrate here that T cells are required for the induction of arthritis; T cell–deficient IL-1Ra –/– mice did not develop arthritis, and transfer of IL-1Ra –/– T cells induced arthritis in nu/nu mice. Development of arthritis was also markedly suppressed by TNF-α deficiency. We found that TNF-α induced OX40 expression on T cells and blocking the interaction between either CD40 and its ligand or OX40 and its ligand suppressed development of arthritis. These findings suggest that IL-1 receptor antagonist deficiency in T cells disrupts homeostasis of the immune system and that TNF-α plays an important role in activating T cells through induction of OX40.</abstract><pub>American Society for Clinical Investigation</pub><pmid>15578092</pmid><doi>10.1172/JCI200420742</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0021-9738
ispartof The Journal of clinical investigation, 2004-12, Vol.114 (11), p.1603-1611
issn 0021-9738
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_529278
source EZB-FREE-00999 freely available EZB journals; PubMed Central
title TNF-α is crucial for the development of autoimmune arthritis in IL-1 receptor antagonist–deficient mice
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T14%3A56%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmedcentral&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TNF-%CE%B1%20is%20crucial%20for%20the%20development%20of%20autoimmune%20arthritis%20in%20IL-1%20receptor%20antagonist%E2%80%93deficient%20mice&rft.jtitle=The%20Journal%20of%20clinical%20investigation&rft.au=Horai,%20Reiko&rft.date=2004-12-01&rft.volume=114&rft.issue=11&rft.spage=1603&rft.epage=1611&rft.pages=1603-1611&rft.issn=0021-9738&rft_id=info:doi/10.1172/JCI200420742&rft_dat=%3Cpubmedcentral%3Epubmedcentral_primary_oai_pubmedcentral_nih_gov_529278%3C/pubmedcentral%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-p177t-82f62894d41f0215ae8bcda856470c0d70c146038c381ac25fd4385baf9e21f03%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/15578092&rfr_iscdi=true