Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
1995-2-27
|
pubmed:abstractText |
Analysis of experimental animal models and human clinical samples has indicated that the selective activation of CD4+ T cell subsets with distinct profiles of cytokine production plays an important role in the pathogenesis of human inflammatory and allergic diseases. The possibility that differential activation of costimulatory pathways is a mechanism for selectively modulating cytokine production by CD4+ T cells was tested. The proliferative response and cytokines secreted by a panel of human CD4+ T cell clones, representative of Th1 or Th2/0 cells, in response to activation of different costimulatory pathways was measured. CD28-mediated costimulatory signals induced proliferation and IFN-gamma secretion by Th1 cells. Although CD28-ligation induced Th2/0 cells to proliferate, it did not trigger IL-4 production. Ligation of LFA-1 and CD45 isoforms also generated costimulatory signals activating cytokine secretion by the different types of T cell clones. Th1 cells secreted the same profile of cytokines, irrespective of which costimulatory pathway was engaged. However, the cytokine secreted by a subset of Th2/0 cells varied, depending upon which costimulatory pathways were activated. These results suggest that the costimulatory pathways activated by APCs can selectively influence cytokine production by CD4+ T cell subsets.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0022-1767
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
154
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1684-90
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:7836752-Animals,
pubmed-meshheading:7836752-Antigens, CD28,
pubmed-meshheading:7836752-Antigens, CD3,
pubmed-meshheading:7836752-Cats,
pubmed-meshheading:7836752-Humans,
pubmed-meshheading:7836752-Hypersensitivity, Immediate,
pubmed-meshheading:7836752-Interferon-gamma,
pubmed-meshheading:7836752-Interleukin-4,
pubmed-meshheading:7836752-Lyme Disease,
pubmed-meshheading:7836752-Lymphocyte Activation,
pubmed-meshheading:7836752-Lymphokines,
pubmed-meshheading:7836752-Mites,
pubmed-meshheading:7836752-Signal Transduction,
pubmed-meshheading:7836752-Th1 Cells,
pubmed-meshheading:7836752-Th2 Cells
|
pubmed:year |
1995
|
pubmed:articleTitle |
Costimulatory signals can selectively modulate cytokine production by subsets of CD4+ T cells.
|
pubmed:affiliation |
Department of Leukocyte Biology, Syntex Research, Palo Alto, CA 94303.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|