Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)

Numerous evidence demonstrate Type 1 diabetes (T1D) is due to a loss of immune tolerance to islet antigens, and CD8 super(+ T cells play an important role in the development of T1D in NOD mice. The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance, howev...

Full description

Saved in:
Bibliographic Details
Published in:Vaccine 2011-10, Vol.29 (44), p.7747-7751
Main Authors: Li, Shufa, Zhang, Min, Xiang, Fei, Zhao, Jianyong, Jiang, Chao, Zhu, Jinkun
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 7751
container_issue 44
container_start_page 7747
container_title Vaccine
container_volume 29
creator Li, Shufa
Zhang, Min
Xiang, Fei
Zhao, Jianyong
Jiang, Chao
Zhu, Jinkun
description Numerous evidence demonstrate Type 1 diabetes (T1D) is due to a loss of immune tolerance to islet antigens, and CD8 super(+ T cells play an important role in the development of T1D in NOD mice. The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance, however, its role in autoimmune diabetes is unknown. To explore whether the generation of tolerance aiming at BTLA will help therapeutic intervention in T1D, the NOD mice were treated with genetically modified dendritic cells (DCs) expressing BTLA. The results demonstrated that transfer of modified DCs significantly induced CD8) super(+) T cell tolerance and attenuated the severity of diabetes. The findings suggest that genetically modified DC therapies enhancing the BTLA negative cosignal may prove valuable in treating T1D and other autoimmune diseases.
doi_str_mv 10.1016/j.vaccine.2011.07.125
format article
fullrecord <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_miscellaneous_902369487</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>902369487</sourcerecordid><originalsourceid>FETCH-proquest_miscellaneous_9023694873</originalsourceid><addsrcrecordid>eNqNzL1uwjAUhmEPReKnXALS2doK4R4nIZCRAlWHjhm6IeMcWqPgpD42au--oeICmL7he_QKMVEoFar8-SjP2hjrSCaolMSFVMn8TgwwybNZpvCjL4bMR0Scp6oYiNOGXOVtsAYM1TUD_bSemK37hJfyfQXWVdEQw3qzBI4t-ccplP8WQlOT184QaFeBDoFc1KGz4YuA6Uxd9xeaA1RW76k7nu5F76BrpvF1R-LhdVuu32atb74jcdidLF_a2lETeVdgkuZFtlykt8s_g4hTJw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>902369487</pqid></control><display><type>article</type><title>Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)</title><source>Elsevier</source><creator>Li, Shufa ; Zhang, Min ; Xiang, Fei ; Zhao, Jianyong ; Jiang, Chao ; Zhu, Jinkun</creator><creatorcontrib>Li, Shufa ; Zhang, Min ; Xiang, Fei ; Zhao, Jianyong ; Jiang, Chao ; Zhu, Jinkun</creatorcontrib><description>Numerous evidence demonstrate Type 1 diabetes (T1D) is due to a loss of immune tolerance to islet antigens, and CD8 super(+ T cells play an important role in the development of T1D in NOD mice. The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance, however, its role in autoimmune diabetes is unknown. To explore whether the generation of tolerance aiming at BTLA will help therapeutic intervention in T1D, the NOD mice were treated with genetically modified dendritic cells (DCs) expressing BTLA. The results demonstrated that transfer of modified DCs significantly induced CD8) super(+) T cell tolerance and attenuated the severity of diabetes. The findings suggest that genetically modified DC therapies enhancing the BTLA negative cosignal may prove valuable in treating T1D and other autoimmune diseases.</description><identifier>ISSN: 0264-410X</identifier><identifier>DOI: 10.1016/j.vaccine.2011.07.125</identifier><language>eng</language><ispartof>Vaccine, 2011-10, Vol.29 (44), p.7747-7751</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Li, Shufa</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><creatorcontrib>Xiang, Fei</creatorcontrib><creatorcontrib>Zhao, Jianyong</creatorcontrib><creatorcontrib>Jiang, Chao</creatorcontrib><creatorcontrib>Zhu, Jinkun</creatorcontrib><title>Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)</title><title>Vaccine</title><description>Numerous evidence demonstrate Type 1 diabetes (T1D) is due to a loss of immune tolerance to islet antigens, and CD8 super(+ T cells play an important role in the development of T1D in NOD mice. The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance, however, its role in autoimmune diabetes is unknown. To explore whether the generation of tolerance aiming at BTLA will help therapeutic intervention in T1D, the NOD mice were treated with genetically modified dendritic cells (DCs) expressing BTLA. The results demonstrated that transfer of modified DCs significantly induced CD8) super(+) T cell tolerance and attenuated the severity of diabetes. The findings suggest that genetically modified DC therapies enhancing the BTLA negative cosignal may prove valuable in treating T1D and other autoimmune diseases.</description><issn>0264-410X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqNzL1uwjAUhmEPReKnXALS2doK4R4nIZCRAlWHjhm6IeMcWqPgpD42au--oeICmL7he_QKMVEoFar8-SjP2hjrSCaolMSFVMn8TgwwybNZpvCjL4bMR0Scp6oYiNOGXOVtsAYM1TUD_bSemK37hJfyfQXWVdEQw3qzBI4t-ccplP8WQlOT184QaFeBDoFc1KGz4YuA6Uxd9xeaA1RW76k7nu5F76BrpvF1R-LhdVuu32atb74jcdidLF_a2lETeVdgkuZFtlykt8s_g4hTJw</recordid><startdate>20111013</startdate><enddate>20111013</enddate><creator>Li, Shufa</creator><creator>Zhang, Min</creator><creator>Xiang, Fei</creator><creator>Zhao, Jianyong</creator><creator>Jiang, Chao</creator><creator>Zhu, Jinkun</creator><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20111013</creationdate><title>Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)</title><author>Li, Shufa ; Zhang, Min ; Xiang, Fei ; Zhao, Jianyong ; Jiang, Chao ; Zhu, Jinkun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_miscellaneous_9023694873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Shufa</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><creatorcontrib>Xiang, Fei</creatorcontrib><creatorcontrib>Zhao, Jianyong</creatorcontrib><creatorcontrib>Jiang, Chao</creatorcontrib><creatorcontrib>Zhu, Jinkun</creatorcontrib><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Vaccine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Shufa</au><au>Zhang, Min</au><au>Xiang, Fei</au><au>Zhao, Jianyong</au><au>Jiang, Chao</au><au>Zhu, Jinkun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)</atitle><jtitle>Vaccine</jtitle><date>2011-10-13</date><risdate>2011</risdate><volume>29</volume><issue>44</issue><spage>7747</spage><epage>7751</epage><pages>7747-7751</pages><issn>0264-410X</issn><abstract>Numerous evidence demonstrate Type 1 diabetes (T1D) is due to a loss of immune tolerance to islet antigens, and CD8 super(+ T cells play an important role in the development of T1D in NOD mice. The novel coinhibitory receptor BTLA may have a regulatory role in maintaining peripheral tolerance, however, its role in autoimmune diabetes is unknown. To explore whether the generation of tolerance aiming at BTLA will help therapeutic intervention in T1D, the NOD mice were treated with genetically modified dendritic cells (DCs) expressing BTLA. The results demonstrated that transfer of modified DCs significantly induced CD8) super(+) T cell tolerance and attenuated the severity of diabetes. The findings suggest that genetically modified DC therapies enhancing the BTLA negative cosignal may prove valuable in treating T1D and other autoimmune diseases.</abstract><doi>10.1016/j.vaccine.2011.07.125</doi></addata></record>
fulltext fulltext
identifier ISSN: 0264-410X
ispartof Vaccine, 2011-10, Vol.29 (44), p.7747-7751
issn 0264-410X
language eng
recordid cdi_proquest_miscellaneous_902369487
source Elsevier
title Dendritic cells expressing BTLA induces CD8 super(+ T cell tolerance and attenuates the severity of diabetes)
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T13%3A04%3A30IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Dendritic%20cells%20expressing%20BTLA%20induces%20CD8%20super(+%20T%20cell%20tolerance%20and%20attenuates%20the%20severity%20of%20diabetes)&rft.jtitle=Vaccine&rft.au=Li,%20Shufa&rft.date=2011-10-13&rft.volume=29&rft.issue=44&rft.spage=7747&rft.epage=7751&rft.pages=7747-7751&rft.issn=0264-410X&rft_id=info:doi/10.1016/j.vaccine.2011.07.125&rft_dat=%3Cproquest%3E902369487%3C/proquest%3E%3Cgrp_id%3Ecdi_FETCH-proquest_miscellaneous_9023694873%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=902369487&rft_id=info:pmid/&rfr_iscdi=true