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Conference Paper: Intrinsic IFN-gamma-T-bet pathway mediates the generation of Th1-like regulatory T cells induced by CD40-activated B cells

TitleIntrinsic IFN-gamma-T-bet pathway mediates the generation of Th1-like regulatory T cells induced by CD40-activated B cells
Authors
KeywordsMedical sciences
Allergology and immunology
Issue Date2010
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
The 2010 Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), Boston, MA., 24-27 June 2010. In Journal of Immunology, 2010, v. 184 meeting abstracts suppl., abstract no. 145.11 How to Cite?
AbstractThe plasticity of CD4+ T cell is found to be higher than previously thought and might be modified by the cross-talking among different signal pathways. On the other hand, the role of CD40-activated B cells in the differentiation of CD4+ T cell is still on debate and their underlying mechanism for inducing Tregs remains unknown. In this study, using coculture of human naïve CD4+CD25- T cells with allogeneic CD40-activated B cells without any exogenous cytokines, we have demonstrated that CD40-activated B cells could induce alloantigen-specific CD4hiCD25hi Tregs and Th1 cells from their naïve precursors under weak and optimal activation respectively. Interestingly, the induced CD4hiCD25hi Tregs had Th1 properties with high level of T-bet expression, and some of them produced IFN-gamma. Both IFN-gamma+ and IFN-gamma-CD4hiCD25hi Tregs had a similar alloantigen-specific suppressive capacity. Importantly, we further found that the endogenously produced IFN-gamma and intrinsic T-bet expression were involved in the generation of these CD4hiCD25hi Tregs but did not mediate their suppression by neutralization of IFN-gamma and interference of T-bet expression with siRNA. We concluded that the generation of these Th1-like Tregs was mediated by IFN-gamma-T-bet pathway and the stimulatory or tolerogenic role of CD40-activated B cells in CD4+ T-cell differentiation was dependent on the strength of the activation to T cells.
DescriptionPoster session - FOCIS Pillar: Immunogenetics/Genomics: S.110
Persistent Identifierhttp://hdl.handle.net/10722/126846
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549

 

DC FieldValueLanguage
dc.contributor.authorTu, Wen_HK
dc.contributor.authorZheng, Jen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-10-31T12:52:00Z-
dc.date.available2010-10-31T12:52:00Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 2010 Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), Boston, MA., 24-27 June 2010. In Journal of Immunology, 2010, v. 184 meeting abstracts suppl., abstract no. 145.11en_HK
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/126846-
dc.descriptionPoster session - FOCIS Pillar: Immunogenetics/Genomics: S.110-
dc.description.abstractThe plasticity of CD4+ T cell is found to be higher than previously thought and might be modified by the cross-talking among different signal pathways. On the other hand, the role of CD40-activated B cells in the differentiation of CD4+ T cell is still on debate and their underlying mechanism for inducing Tregs remains unknown. In this study, using coculture of human naïve CD4+CD25- T cells with allogeneic CD40-activated B cells without any exogenous cytokines, we have demonstrated that CD40-activated B cells could induce alloantigen-specific CD4hiCD25hi Tregs and Th1 cells from their naïve precursors under weak and optimal activation respectively. Interestingly, the induced CD4hiCD25hi Tregs had Th1 properties with high level of T-bet expression, and some of them produced IFN-gamma. Both IFN-gamma+ and IFN-gamma-CD4hiCD25hi Tregs had a similar alloantigen-specific suppressive capacity. Importantly, we further found that the endogenously produced IFN-gamma and intrinsic T-bet expression were involved in the generation of these CD4hiCD25hi Tregs but did not mediate their suppression by neutralization of IFN-gamma and interference of T-bet expression with siRNA. We concluded that the generation of these Th1-like Tregs was mediated by IFN-gamma-T-bet pathway and the stimulatory or tolerogenic role of CD40-activated B cells in CD4+ T-cell differentiation was dependent on the strength of the activation to T cells.-
dc.languageengen_HK
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org-
dc.relation.ispartofJournal of Immunology-
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org-
dc.subjectMedical sciences-
dc.subjectAllergology and immunology-
dc.titleIntrinsic IFN-gamma-T-bet pathway mediates the generation of Th1-like regulatory T cells induced by CD40-activated B cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1767&volume=184&issue=Meeting Abstract Suppl.&spage=145.11&epage=&date=2010&atitle=Intrinsic+IFN-gamma-T-bet+pathway+mediates+the+generation+of+Th1-like+regulatory+T+cells+induced+by+CD40-activated+B+cells-
dc.identifier.emailTu, W: wwtu@hkucc.hku.hken_HK
dc.identifier.emailZheng, J: teddybear81@sina.comen_HK
dc.identifier.emailLiu, Y: yinpingl@hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hkucc.hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityLiu, Y=rp00269en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros173900en_HK
dc.identifier.volume184-
dc.identifier.issuemeeting abstracts suppl.-
dc.description.otherThe 2010 Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), Boston, MA., 24-27 June 2010. In Journal of Immunology, 2010, v. 184 meeting abstract suppl., abstract no. 145.11-

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