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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
1998-11-24
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pubmed:abstractText |
Infectious tolerance can be induced in many ways, does not require a thymus or clonal deletion and can spread to third-party antigens linked on the same antigen-presenting cell-the process being variously described as linked-, bystanderor epitope-suppression. We here review the evidence concerning the mechanisms involved and attempt to make a consistent hypothesis, that during tolerance induction in the Th1-mediated autoimmune diseases and transplantation systems there would seem to be a phase of immune deviation towards Th2 cytokines, like IL-4 and IL-10; however, this may lead to an IL-10-induced form of anergy or nonresponsiveness and generation of the recently characterized Th3/T-regulatory-1 CD4+ T cell subset which is thought to downregulate the antigen-presenting cell, possibly via transforming growth factor beta.
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pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0952-7915
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
10
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
518-24
|
pubmed:dateRevised |
2005-11-16
|
pubmed:meshHeading | |
pubmed:year |
1998
|
pubmed:articleTitle |
Infectious tolerance.
|
pubmed:affiliation |
Sir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, UK. stephen.cobbold@pathology.ox.ac.uk
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pubmed:publicationType |
Journal Article,
Review
|