Linked Life Data

15463673

Source:http://linkedlifedata.com/resource/pubmed/id/15463673

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2004-10-6
pubmed:abstractText
Burnet and Fenner originally defined 'tolerance' as 'unresponsiveness against self'. It is now generally accepted that the phenomenon of tolerance is required to protect on individual from potentially autoreactive cells. Recent experiments have independently shown that parasite infection or interleukin 2 (IL-2) can reverse an established T-cell tolerance in vivo. Breaking T-cell tolerance restores the capacity of T cells to be stimulated by their specific antigen and, in the case of a self-antigen, may be followed by autoimmune disease. In this review, Martin Röcken and Ethan Shevach briefly describe the potential pathways for generating T-cell tolerance in vivo, and focus on recently described mechanisms by which parasitic infections may circumvent or abrogate the tolerant state.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Oct
pubmed:issn
0169-4758
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
377-80
pubmed:year
1993
pubmed:articleTitle
Do parasitic infections break T-cell tolerance and trigger autoimmune disease?
pubmed:affiliation
Laboratory of Immunology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article