Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2002-6-10
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
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
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6263-72
pubmed:dateRevised
2009-11-19
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
pubmed:year
2002
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.
pubmed:affiliation
Department of Immunology and Medical Zoology, School of Medicine, Kagoshima University, Sakuragaoka, Kagoshima, Japan. katusaki@m3.kufm.kagoshima-u.ac.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't