Document Detail

T-T cellular interaction between CD4-CD8- regulatory T cells and T cell clones presenting TCR peptide. Its implication for TCR vaccination against experimental autoimmune encephalomyelitis.
MedLine Citation:
PMID:  8759768     Owner:  NLM     Status:  MEDLINE    
Regulatory T cells recognizing TCR determinants presumably play a critical role in the control of experimental autoimmune encephalomyelitis, a prototype tissue-specific autoimmune disease. This study was initiated to determine whether regulatory T cells can be induced against a V beta 17a CDR2 peptide (residues 50-68) in SJL/J mice. Although the TCR peptide showed regulatory effects in vivo, the presence of T cells specific for the peptide could not be proven with conventional proliferation assays. Unexpectedly, in the presence of myelin basic protein-specific T clone cells (Tcc), the sensitized spleen cells vigorously proliferated in response to the TCR peptide. The subsequent experiment showed that this was due to the outstanding capability of the Tcc as APC for the exogenous TCR peptide. Using the Tcc as APC, we were able to establish V beta 17a50-68-specific T cell lines from in vivo primed spleen cells. The line cells were MHC class I restricted and dominated by T cells with a distinct surface phenotype (CD4-CD8-V beta 17a+). Presentation of the peptide by the Tcc was inhibited by treatment with gelonin that could block a MHC class I presentation pathway. The ability of T cells to present the TCR peptide was not related to their Ag specificity, but correlated with the expression levels of MHC class I molecules and adhesion molecules such as intercellular adhesion molecule-1 and B7-1 on their surface. The TCR peptide-specific T cells produced a soluble mediator(s) that is inhibitory for T cell activation and were protective against actively induced experimental autoimmune encephalomyelitis. These results show that V beta 17a50-68 vaccination induces regulatory CD4-CD8- T cells that could interact with T cells presenting relevant TCR fragments.
M F Kozovska; T Yamamura; T Tabira
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  157     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-09-17     Completed Date:  1996-09-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1781-90     Citation Subset:  AIM; IM    
Department of Demyelinating Disease and Aging, National Center of Neurology and Psychiatry, Tokyo, Japan.
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MeSH Terms
Amino Acid Sequence
Antigens, CD4 / analysis
Antigens, CD8 / analysis
Antigens, CD80 / physiology
Autoimmune Diseases / immunology*
Clone Cells / metabolism
Encephalomyelitis, Autoimmune, Experimental / immunology*
Intercellular Adhesion Molecule-1 / physiology
Lymphocyte Activation
Molecular Sequence Data
Plant Proteins / pharmacology
Receptors, Antigen, T-Cell / immunology*
Ribosome Inactivating Proteins, Type 1
Specific Pathogen-Free Organisms
T-Lymphocyte Subsets / immunology*
Reg. No./Substance:
0/Antigens, CD4; 0/Antigens, CD8; 0/Antigens, CD80; 0/Plant Proteins; 0/Receptors, Antigen, T-Cell; 0/Ribosome Inactivating Proteins, Type 1; 126547-89-5/Intercellular Adhesion Molecule-1; 75037-46-6/GEL protein, Gelonium multiflorum

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