|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
3
|
|
pubmed:dateCreated |
2005-1-21
|
|
pubmed:abstractText |
In this study we examined the role and regulation of OX40 signals during CD4 T cell priming on dendritic cells (DCs). Contrary to expectation, OX40-deficient cells proliferated more rapidly than their normal counterparts, particularly when stimulated with peptide in the absence of added cytokines. This proliferative advantage was not apparent for Th2-differentiated cells. When the reasons for this were investigated, we found that the cytokine IL-4 specifically down-regulated expression of OX40 ligand on T, B, and DCs, but not on the CD4(+)CD3(-) cells linked with selection of Th2 cells into the memory compartment. OX40 ligand expression was also down-regulated on rapidly proliferating Th1 effectors. These data are compatible with OX40 signals acting during priming as a check on naive T cell proliferation while T cells integrate additional DC signals. This would serve to limit inappropriate T cell responses. In contrast, OX40 signals from CD4(+)CD3(-) cells located in the outer T zone select proliferating Th2 effectors into the memory T cell pool.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, OX40,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfrsf4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factors
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Feb
|
|
pubmed:issn |
0022-1767
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
174
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1433-7
|
|
pubmed:dateRevised |
2007-8-13
|
|
pubmed:meshHeading |
pubmed-meshheading:15661901-Animals,
pubmed-meshheading:15661901-Antigens, CD3,
pubmed-meshheading:15661901-B-Lymphocytes,
pubmed-meshheading:15661901-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15661901-Cell Differentiation,
pubmed-meshheading:15661901-Cell Division,
pubmed-meshheading:15661901-Cell Proliferation,
pubmed-meshheading:15661901-Cells, Cultured,
pubmed-meshheading:15661901-Dendritic Cells,
pubmed-meshheading:15661901-Down-Regulation,
pubmed-meshheading:15661901-Growth Inhibitors,
pubmed-meshheading:15661901-Interleukin-4,
pubmed-meshheading:15661901-Ligands,
pubmed-meshheading:15661901-Lymphocyte Activation,
pubmed-meshheading:15661901-Membrane Glycoproteins,
pubmed-meshheading:15661901-Mice,
pubmed-meshheading:15661901-Mice, Inbred C57BL,
pubmed-meshheading:15661901-Mice, Knockout,
pubmed-meshheading:15661901-Mice, Transgenic,
pubmed-meshheading:15661901-Receptors, OX40,
pubmed-meshheading:15661901-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:15661901-Signal Transduction,
pubmed-meshheading:15661901-Th1 Cells,
pubmed-meshheading:15661901-Th2 Cells,
pubmed-meshheading:15661901-Tumor Necrosis Factors
|
|
pubmed:year |
2005
|
|
pubmed:articleTitle |
OX40 signals during priming on dendritic cells inhibit CD4 T cell proliferation: IL-4 switches off OX40 signals enabling rapid proliferation of Th2 effectors.
|
|
pubmed:affiliation |
Medical Research Council Centre for Immune Regulation, Birmingham Medical School, Birmingham, United Kingdom.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
