Linked Life Data

9050744

Source:http://linkedlifedata.com/resource/pubmed/id/9050744

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-6-24
pubmed:abstractText
Interleukin 10 (IL-10) is a pleiotropic T cell-derived cytokine best known for its negative regulatory effects on T cell immunity. It inhibits responses indirectly by downregulating expression of major histocompatibility complex (MHC) molecules and co-stimulatory molecules such as CD80 on antigen presenting cells as well as directly via its effects on responding cells. On the other hand, IL-10 has been shown to protect activated T cells against apoptosis caused by withdrawal of the major growth factor, IL-2, and allow proliferation of T cells in the absence of IL-2. However, we show here that this IL-10-dependent, IL-2-independent proliferative response is short-lived, and that IL-10-responsive T cells cannot multiply in its presence. Moreover, inclusion of exogenous IL-10 in clonal cultures propagated with IL-2 results in suppression of their growth. These findings, together with the observation that IL-10 fails to protect T cells against activation-induced cell death (a fas/fas-ligand-dependent phenomenon blocked only by certain antagonistic anti-fas reagents), suggest that the negative regulatory effects of IL-10 outweigh the upregulated proliferation observed on some T cell clones (TCC) in the absence of IL-2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1043-4666
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
877-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Interleukin 10 protects activated human T lymphocytes against growth factor withdrawal-induced cell death but only anti-fas antibody can prevent activation-induced cell death.
pubmed:affiliation
Second Department of Internal Medicine, University of Tübingen MedicalSchool, Federal Republic of Germany. graham.pawelec@uni-tuebingen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't