Linked Life Data

1535516

Source:http://linkedlifedata.com/resource/pubmed/id/1535516

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-8-4
pubmed:abstractText
Pancreatic beta-cell autoantigen recognition by the immune system appears to be a critical event in the evolution of insulin dependent diabetes. Immune recognition involves antigen presentation by macrophages and subsequent antigen-peptide-class II MHC recognition by T cell receptors (TCR). Using the NOD mouse as a model for human IDD, we hypothesized that germline variability in the D beta nod and/or J beta nod segments could contribute to beta cell autoimmunity by influencing the specific peptides that are recognized. As an initial approach to our hypothesis, we sought to compare these segments to other strains of mice in search of genetic polymorphisms as reported in NZW mice. The germ line TCR beta nod gene did not display evidence of an expansion or contraction in the number of D beta nod or J beta nod segments at the level of resolution provided by restriction fragment length polymorphism analysis. The absence of such polymorphisms suggests that D beta nod or J beta nod segments are not different from nonautoimmune strains of mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0891-6934
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-12
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
T cell receptor beta diversity and joining segments in the NOD mouse.
pubmed:affiliation
University of Florida College of Medicine, Department of Pathology and Laboratory Medicine, Gainesville 32610.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't