Linked Life Data

11801642

Source:http://linkedlifedata.com/resource/pubmed/id/11801642

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-1-21
pubmed:abstractText
Progesterone may contribute to the maternal suppression of immunity to the fetus by modulating the Th1/Th2 balance. To clarify whether progesterone directly or indirectly affects T cell differentiation, we used two experimental systems with isolated T cells in vitro. In one system, isolated CD4+CD8+thymocytes differentiated into Th1 and Th2 by two pulse stimulations with defined combinations of ionomycin and PMA followed by the treatment with IL-12, IL-4, and IL-2. In the second system, functional differentiation was induced in purified naive CD4 T cells with cytokines and Abs to CD3 and CD28. In both systems, progesterone added with cytokines suppressed Th1 development at concentrations associated with pregnancy, but enhanced the development of IL-10-producing Th2 cells. Because IL-10 is known to inhibit APC production of IL-12, Th1 development may be also suppressed indirectly by progesterone. However, progesterone failed to enhance IL-10 production in the absence of IL-12. The p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 inhibited Th1 development and enhanced Th2 development, as did progesterone, indicating that p38 MAPK and extracellular signal-regulated kinase pathways are involved in Th1 development. However, the progesterone effects may not be simply due to a modulation of MAPK activities, because the inhibitor did not significantly affect the development of IL-10-producing cells in the presence or absence of progesterone. Glucocorticoids exerted effects similar to those of progesterone on Th1/Th2 development even at lower concentrations. These results suggest that progesterone as well as glucocorticoids directly inhibit Th1 development and enhance Th2 development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1087-94
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11801642-Adjuvants, Immunologic, pubmed-meshheading:11801642-Animals, pubmed-meshheading:11801642-Cell Culture Techniques, pubmed-meshheading:11801642-Cell Differentiation, pubmed-meshheading:11801642-Cells, Cultured, pubmed-meshheading:11801642-Corticosterone, pubmed-meshheading:11801642-Enzyme Inhibitors, pubmed-meshheading:11801642-Glucocorticoids, pubmed-meshheading:11801642-Growth Inhibitors, pubmed-meshheading:11801642-Immunosuppressive Agents, pubmed-meshheading:11801642-Interleukin-10, pubmed-meshheading:11801642-Interleukin-4, pubmed-meshheading:11801642-Male, pubmed-meshheading:11801642-Mice, pubmed-meshheading:11801642-Mice, Inbred C57BL, pubmed-meshheading:11801642-Mice, Knockout, pubmed-meshheading:11801642-Mitogen-Activated Protein Kinases, pubmed-meshheading:11801642-Progesterone, pubmed-meshheading:11801642-Th1 Cells, pubmed-meshheading:11801642-Th2 Cells, pubmed-meshheading:11801642-p38 Mitogen-Activated Protein Kinases
pubmed:year
2002
pubmed:articleTitle
Direct and indirect inhibition of Th1 development by progesterone and glucocorticoids.
pubmed:affiliation
Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida-shi, Tokyo 194-8511, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't