Source:http://linkedlifedata.com/resource/pubmed/id/11722623
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2001-11-27
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pubmed:abstractText |
Depletion of the minor ( approximately 10%) subpopulation of CD4+ T cells that co-expresses CD25 (interleukin (IL)-2 receptor alpha-chain) by thymectomy of neonates on the third day of life or by treatment of adult CD4+ T cells with anti-CD25 and complement results in the development of organ-specific autoimmunity. Autoimmune disease can be prevented by reconstitution of the animals with CD4+ CD25+ cells. CD4+ CD25+-mediated protection of autoimmune gastritis does not require the suppressor cytokines IL-4, IL-10, or transforming growth factor (TGF)-beta. Mice that express a transgenic T-cell receptor (TCR) derived from a thymectomized newborn that recognizes the gastric parietal cell antigen H/K ATPase all develop severe autoimmune gastritis very early in life. CD4+ CD25+ T cells are also powerful suppressors of the activation of both CD4+ and CD8+ T cells in vitro. Suppression is mediated by a cell contact-dependent, cytokine-independent T-T interaction. Activation of CD4+ CD25+ via their TCR generates suppressor effector cells that are capable of non-specifically suppressing the activation of any CD4+ or CD8+ T cell. Activation of suppressor effector function is independent of co-stimulation mediated by CD28/CTLA-4 interactions with CD80/CD86. We propose that CD4+ CD25+ T cells recognize organ-specific antigens, are recruited to sites of autoimmune damage where they are activated by their target antigen, and then physically interact with autoreactive CD4+ or CD8+ effector cells to suppress the development of autoimmune disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0105-2896
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
182
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
58-67
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:11722623-Animals,
pubmed-meshheading:11722623-Autoimmune Diseases,
pubmed-meshheading:11722623-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11722623-Cell Division,
pubmed-meshheading:11722623-Humans,
pubmed-meshheading:11722623-Lymphocyte Activation,
pubmed-meshheading:11722623-Organ Specificity,
pubmed-meshheading:11722623-Receptors, Antigen, T-Cell,
pubmed-meshheading:11722623-Receptors, Interleukin-2,
pubmed-meshheading:11722623-T-Lymphocytes, Regulatory,
pubmed-meshheading:11722623-Thymus Gland,
pubmed-meshheading:11722623-Transgenes
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pubmed:year |
2001
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pubmed:articleTitle |
Control of T-cell activation by CD4+ CD25+ suppressor T cells.
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pubmed:affiliation |
Cellular Immunology Section, Laboratory of Immunology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ems1@mail.nih.gov
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pubmed:publicationType |
Journal Article,
Review
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