Source:http://linkedlifedata.com/resource/pubmed/id/14764692
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
2004-2-6
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| pubmed:abstractText |
Several classes of anergic T cells are capable of suppressing naive T cell proliferation and thereby limiting immune responses. Activated T cells, although not anergic, are transiently refractory to restimulation with Ag. We examine in this study whether activated refractory murine T cells can also suppress naive T cell responses. We find that they can, and that they exhibit many of the suppressive properties of anergic T cells. The activated cells strongly diminish Ag-mediated T cell proliferation, an activity that correlates with their refractory period. Suppression is independent of APC numbers and requires cell contact or proximity. Naive T cells stimulated in the presence of activated refractory cells up-regulate CD25 and CD69, but fail to produce IL-2. The addition of IL-2 to culture medium, however, does not prevent the suppression, which is therefore not solely due to the absence of this growth factor. Persistence of the suppressor cells is also not essential. T cells stimulated in their presence and then isolated from them and cultured do not divide. The suppressive cells, however, do not confer a refractory or anergic state on the target T lymphocytes, which can fully respond to antigenic stimulation if removed from the suppressors. Our results therefore provide evidence that activated T cells act as transient suppressor cells, severely constraining bystander T cell stimulation and thereby restricting their response. These results have potentially broad implications for the development and regulation of immune responses.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
|
| pubmed:volume |
172
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2238-46
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:14764692-Amino Acid Sequence,
pubmed-meshheading:14764692-Animals,
pubmed-meshheading:14764692-Cell Communication,
pubmed-meshheading:14764692-Cell Division,
pubmed-meshheading:14764692-Cells, Cultured,
pubmed-meshheading:14764692-Clonal Anergy,
pubmed-meshheading:14764692-Coculture Techniques,
pubmed-meshheading:14764692-Epitopes, T-Lymphocyte,
pubmed-meshheading:14764692-G0 Phase,
pubmed-meshheading:14764692-G1 Phase,
pubmed-meshheading:14764692-Interleukin-2,
pubmed-meshheading:14764692-Interphase,
pubmed-meshheading:14764692-Lymphocyte Activation,
pubmed-meshheading:14764692-Major Histocompatibility Complex,
pubmed-meshheading:14764692-Mice,
pubmed-meshheading:14764692-Mice, Inbred C57BL,
pubmed-meshheading:14764692-Mice, Inbred DBA,
pubmed-meshheading:14764692-Mice, Transgenic,
pubmed-meshheading:14764692-Molecular Sequence Data,
pubmed-meshheading:14764692-T-Lymphocyte Subsets,
pubmed-meshheading:14764692-T-Lymphocytes, Regulatory
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Antigen nonspecific suppression of T cell responses by activated stimulation-refractory CD4+ T cells.
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| pubmed:affiliation |
Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|