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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0039194,
umls-concept:C0086418,
umls-concept:C0178719,
umls-concept:C0185117,
umls-concept:C0205148,
umls-concept:C0337112,
umls-concept:C0599896,
umls-concept:C0851285,
umls-concept:C1524075,
umls-concept:C2911684
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pubmed:issue |
1
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pubmed:dateCreated |
2000-1-19
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pubmed:abstractText |
The surface and cytoplasmic expressions of the transducing chain (IFN-gamma R2) of the heterodimeric IFN-gamma receptor on human T lymphocytes have been investigated. We show that its surface expression is low, whereas high cytoplasmic levels are found in both resting and PHA-activated T lymphocytes. This low expression does not prevent activated T cells from responding to IFN-gamma, because it induces IFN-regulatory factor 1 expression. Low surface IFN-gamma R2 expression appears to be due to recycling between cytoplasmic stores and the cell surface, which does not depend on signals mediated by endogenous IFN-gamma, because IFN-gamma R2 surface expression is low, and its internalization is equally observed in patients with inherited IFN-gamma R1 gene deficiency and in healthy donors. Moreover, IFN-gamma R2 internalization in T lymphoblasts from healthy donors was not affected by the presence of anti-IFN-gamma-neutralizing or anti-IFN-gamma R1-blocking mAb. In conclusion, these data illustrate a new mechanism whereby human T cells limit the surface expression of IFN-gamma R2 in a ligand-independent manner.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Clathrin,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/IRF1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept,
http://linkedlifedata.com/resource/pubmed/chemical/interferon gamma receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
164
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
201-7
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:10605012-Antigens, CD,
pubmed-meshheading:10605012-Antigens, Differentiation,
pubmed-meshheading:10605012-Biological Transport,
pubmed-meshheading:10605012-CTLA-4 Antigen,
pubmed-meshheading:10605012-Cell Membrane,
pubmed-meshheading:10605012-Cells, Cultured,
pubmed-meshheading:10605012-Clathrin,
pubmed-meshheading:10605012-Cytoplasm,
pubmed-meshheading:10605012-DNA-Binding Proteins,
pubmed-meshheading:10605012-Endocytosis,
pubmed-meshheading:10605012-Humans,
pubmed-meshheading:10605012-Immunoconjugates,
pubmed-meshheading:10605012-Immunologic Deficiency Syndromes,
pubmed-meshheading:10605012-Interferon Regulatory Factor-1,
pubmed-meshheading:10605012-Interferon-gamma,
pubmed-meshheading:10605012-Interphase,
pubmed-meshheading:10605012-Intracellular Fluid,
pubmed-meshheading:10605012-Lymphocyte Activation,
pubmed-meshheading:10605012-Phosphoproteins,
pubmed-meshheading:10605012-Receptors, Interferon,
pubmed-meshheading:10605012-T-Lymphocytes
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pubmed:year |
2000
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pubmed:articleTitle |
Surface expression of the IFN-gamma R2 chain is regulated by intracellular trafficking in human T lymphocytes.
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pubmed:affiliation |
Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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