Source:http://linkedlifedata.com/resource/pubmed/id/15905518
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2005-5-20
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| pubmed:abstractText |
To date, very few Ag-based regimens have been defined that could expand T regulatory (Treg) cells to reverse autoimmunity. Additional understanding of Treg function with respect to specificity and broad suppression should help overcome these limitations. Ig-proteolipid protein (PLP)1, an Ig carrying a PLP1 peptide corresponding to amino acid residues 139-151 of PLP, displayed potent tolerogenic functions and proved effective against experimental allergic encephalomyelitis (EAE). In this study, we took advantage of the Ig-PLP1 system and the PLP1-specific TCR transgenic 5B6 mouse to define a regimen that could expand Ag-specific Treg cells in vivo and tested for effectiveness against autoimmunity involving diverse T cell specificities. The findings indicate that in vivo exposure to aggregated Ig-PLP1 drives PLP1-specific 5B6 TCR transgenic cells to evolve as Treg cells expressing CD25, CTLA-4, and Foxp3 and producing IL-10. These Treg cells were able to suppress PLP1 peptide-induced EAE in both SJL/J and F(1) (SJL/J x C57BL/6) mice. However, despite being effective against disease induced with a CNS homogenate, the Treg cells were unable to counter EAE induced by a myelin basic protein or a myelin oligodendrocyte glycoprotein peptide. Nevertheless, activation with Ag before transfer into the host mice supports suppression of both myelin oligodendrocyte glycoprotein- and myelin basic protein peptide-induced EAE. Thus, it is suggested that activation of Treg cells by the cognate autoantigen is necessary for operation of broad suppressive functions.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Proteolipid Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/myelin proteolipid protein (139-151)
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
|
| pubmed:issn |
0022-1767
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| pubmed:author |
pubmed-author:BellJ JeremiahJJ,
pubmed-author:CollinsMaryM,
pubmed-author:DivekarRohitR,
pubmed-author:EllisJason SJS,
pubmed-author:GreggRandal KRK,
pubmed-author:HardawayJohn CJC,
pubmed-author:JainRenuR,
pubmed-author:KuchrooVijay KVK,
pubmed-author:LeeHyun-HeeHH,
pubmed-author:WaldnerHanspeterH,
pubmed-author:YuPingP,
pubmed-author:ZaghouaniHabibH
|
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
174
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
6772-80
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| pubmed:dateRevised |
2011-8-26
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| pubmed:meshHeading |
pubmed-meshheading:15905518-Amino Acid Sequence,
pubmed-meshheading:15905518-Animals,
pubmed-meshheading:15905518-Bystander Effect,
pubmed-meshheading:15905518-Cell Proliferation,
pubmed-meshheading:15905518-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:15905518-Epitopes, T-Lymphocyte,
pubmed-meshheading:15905518-Female,
pubmed-meshheading:15905518-Lymphocyte Activation,
pubmed-meshheading:15905518-Male,
pubmed-meshheading:15905518-Mice,
pubmed-meshheading:15905518-Mice, Inbred C57BL,
pubmed-meshheading:15905518-Mice, Knockout,
pubmed-meshheading:15905518-Mice, Transgenic,
pubmed-meshheading:15905518-Molecular Sequence Data,
pubmed-meshheading:15905518-Myelin Proteolipid Protein,
pubmed-meshheading:15905518-Peptide Fragments,
pubmed-meshheading:15905518-Rats,
pubmed-meshheading:15905518-Receptors, Antigen, T-Cell,
pubmed-meshheading:15905518-Recurrence,
pubmed-meshheading:15905518-Severity of Illness Index,
pubmed-meshheading:15905518-T-Lymphocytes, Regulatory
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| pubmed:year |
2005
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| pubmed:articleTitle |
Specific T regulatory cells display broad suppressive functions against experimental allergic encephalomyelitis upon activation with cognate antigen.
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| pubmed:affiliation |
Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, 65212, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, N.I.H., Extramural
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