Document Detail


Silencing T-bet defines a critical role in the differentiation of autoreactive T lymphocytes.
MedLine Citation:
PMID:  15539157     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As a means of developing therapies that target the pathogenic T cells in multiple sclerosis (MS) without compromising the immune system or eliciting systemic side effects, we investigated the use of T-bet-specific antisense oligonucleotides and small interfering RNAs (siRNA) to silence T-bet expression in autoreactive encephalitogenic T cells and evaluated the biological consequences of this suppression in experimental autoimmune encephalomyelitis, a model for MS. The T-bet-specific AS oligonucleotide and siRNA suppressed T-bet expression, IFNgamma production, and STAT1 levels during antigen-specific T cell differentiation. In vitro suppression of T-bet during differentiation of myelin-specific T cells and in vivo administration of a T-bet-specific antisense oligonucleotide or siRNA inhibited disease. T-bet was shown to bind the IFNgamma and STAT1 promoters, but did not regulate the IL-12/STAT4 pathway. Since T-bet regulates IFNgamma production in CD4(+) T cells, but to a lesser extent in most other IFNgamma-producing cells, T-bet may be a target for therapeutics for Th1-mediated diseases.
Authors:
Amy E Lovett-Racke; Anne E Rocchini; Judy Choy; Sara C Northrop; Rehana Z Hussain; Robert B Ratts; Devanjan Sikder; Michael K Racke
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Immunity     Volume:  21     ISSN:  1074-7613     ISO Abbreviation:  Immunity     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-12     Completed Date:  2004-12-15     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9432918     Medline TA:  Immunity     Country:  United States    
Other Details:
Languages:  eng     Pagination:  719-31     Citation Subset:  IM    
Affiliation:
Department of Neurology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390 USA. amy.lovett-racke@utsouthwestern.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation
DNA-Binding Proteins / genetics
Encephalomyelitis, Autoimmune, Experimental / immunology,  therapy
Interferon-gamma / genetics
Interleukin-12 / pharmacology
Mice
Oligonucleotides, Antisense / pharmacology
RNA, Small Interfering / pharmacology
Receptors, Interleukin / genetics
Receptors, Interleukin-12
STAT1 Transcription Factor
STAT4 Transcription Factor
T-Box Domain Proteins
T-Lymphocytes / cytology*
Trans-Activators / genetics
Transcription Factors / genetics,  physiology*
Grant Support
ID/Acronym/Agency:
K24 NS044250/NS/NINDS NIH HHS; R01 NS037513/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Oligonucleotides, Antisense; 0/RNA, Small Interfering; 0/Receptors, Interleukin; 0/Receptors, Interleukin-12; 0/STAT1 Transcription Factor; 0/STAT4 Transcription Factor; 0/Stat1 protein, mouse; 0/Stat4 protein, mouse; 0/T-Box Domain Proteins; 0/T-box transcription factor TBX21; 0/Trans-Activators; 0/Transcription Factors; 187348-17-0/Interleukin-12; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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