rdf:type |
|
lifeskim:mentions |
umls-concept:C0011155,
umls-concept:C0017262,
umls-concept:C0037083,
umls-concept:C0039194,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0332281,
umls-concept:C0441471,
umls-concept:C1332690,
umls-concept:C1332691,
umls-concept:C1332700,
umls-concept:C1332714,
umls-concept:C1579373,
umls-concept:C1710082,
umls-concept:C1879547,
umls-concept:C2911684
|
pubmed:issue |
12
|
pubmed:dateCreated |
2002-6-10
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pubmed:abstractText |
Human memory CD4(+) T cells respond better to inflammatory CCLs/CC chemokines, CCL3 and CCL5, than naive CD4(+) T cells. We analyzed the regulatory mechanism underlying this difference. Memory and naive CD4(+) T cells expressed similarly high levels of CCR1; however, CCR5 was only expressed in memory CD4(+) T cells at low levels. Experiments using mAbs to block chemokine receptors revealed that CCR1 functioned as a major receptor for the binding of CCL5 in memory and naive CD4(+) T cells as well as the ligand-induced chemotaxis in memory CD4(+) T cells. Stimulation of memory CD4(+) T cells with CCL5 activated protein tyrosine kinase-dependent cascades, which were significantly blocked by anti-CCR1 mAb, whereas this stimulation failed to induce these events in naive CD4(+) T cells. Intracellular expressions of regulator of G protein signaling 3 and 4 were only detected in naive CD4(+) T cells. Pretreatment of cell membrane fractions from memory and naive CD4(+) T cells with GTP-gamma S inhibited CCL5 binding, indicating the involvement of G proteins in the interaction of CCL5 and its receptor(s). In contrast, CCL5 enhanced the GTP binding to G(i alpha) and G(q alpha) in memory CD4(+) T cells, but not in naive CD4(+) T cells. Thus, a failure of the ligand-induced activation of CCR1-mediated downstream signaling event as well as a deficiency of CCR5 expression may be involved in the hyporesponsiveness of naive CD4(+) T cells to CCL3 and CCL5.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL5,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine Diphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Heterotrimeric GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RGS Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6263-72
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12055240-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12055240-Cells, Cultured,
pubmed-meshheading:12055240-Chemokine CCL3,
pubmed-meshheading:12055240-Chemokine CCL4,
pubmed-meshheading:12055240-Chemokine CCL5,
pubmed-meshheading:12055240-Chemotaxis, Leukocyte,
pubmed-meshheading:12055240-Guanosine Diphosphate,
pubmed-meshheading:12055240-Guanosine Triphosphate,
pubmed-meshheading:12055240-Heterotrimeric GTP-Binding Proteins,
pubmed-meshheading:12055240-Humans,
pubmed-meshheading:12055240-Immune Tolerance,
pubmed-meshheading:12055240-Immunologic Memory,
pubmed-meshheading:12055240-Interphase,
pubmed-meshheading:12055240-Ligands,
pubmed-meshheading:12055240-Lymphocyte Activation,
pubmed-meshheading:12055240-Macrophage Inflammatory Proteins,
pubmed-meshheading:12055240-Protein Binding,
pubmed-meshheading:12055240-RGS Proteins,
pubmed-meshheading:12055240-Receptors, CCR1,
pubmed-meshheading:12055240-Receptors, CCR5,
pubmed-meshheading:12055240-Receptors, Chemokine,
pubmed-meshheading:12055240-Signal Transduction,
pubmed-meshheading:12055240-T-Lymphocyte Subsets
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pubmed:year |
2002
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pubmed:articleTitle |
An abortive ligand-induced activation of CCR1-mediated downstream signaling event and a deficiency of CCR5 expression are associated with the hyporesponsiveness of human naive CD4+ T cells to CCL3 and CCL5.
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pubmed:affiliation |
Department of Immunology and Medical Zoology, School of Medicine, Kagoshima University, Sakuragaoka, Kagoshima, Japan. katusaki@m3.kufm.kagoshima-u.ac.jp
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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