Linked Life Data

11396094

Source:http://linkedlifedata.com/resource/pubmed/id/11396094

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-6-8
pubmed:abstractText
The mechanistic basis for HLA associations with RA is still unknown in spite of 20 years of disease association studies and a detailed characterization of HLA class II alleles associated with disease. Analysis of the structural interactions between DR4 susceptibility molecules and T cells specific for the peptide-MHC complex suggests a mechanism for directed T-cell selection and amplification in which RA-associated genetic polymorphisms bias intermolecular recognition. New immunologic models for illustrating the importance of regulated thresholds for T-cell activation based on avidity between the TCR, MHC, and peptide offer insight into a potential mechanism in which the disease-associated HLA molecules create an autoimmune-prone individual by virtue of a biased TCR selection and T-cell amplification process. New tools such as the use of HLA-DR4 tetramers provide the ability to identify and monitor the presence of such autoreactive T cells in the periphery of individuals and patients and should assist in further testing of the multistep model for RA pathways presented in this article.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0889-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
305-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
The role of the DR4 shared epitope in selection and commitment of autoreactive T cells in rheumatoid arthritis.
pubmed:affiliation
Virginia Mason Research Center, Seattle, Washington, USA. nepom@vmresearch.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't