Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-7-13
pubmed:abstractText
Type 1 diabetes is the result of destruction of the insulin-secreting beta-cells of the pancreas by a process in which T-cells play a central role. A tyrosine phosphatase-like protein, IA-2, is a major target for autoantibodies and T-cells in the disease. In this study, we have further characterized the T-cell response to IA-2 by the generation and characterization of T-cell lines. T-cell lines responsive to IA-2 antigen were generated from 17 of 32 patients and 3 of 10 control subjects. Antigen specificity was confirmed in lines from six diabetic patients and one control individual by demonstration of responses to synthetic IA-2 peptides and epitope mapping. Five lines from diabetic patients responded to one of two peptides representing amino acids 831-850 and 841-860 of IA-2. The overlapping portion may therefore represent an immunodominant region of the molecule. The sixth patient-derived line responded to a peptide representing amino acids 751-770 of IA-2 presented by the DR 4 (DRB1*0401) allele that confers susceptibility to type 1 diabetes. Primary T-cell responses to peptides of the immunodominant region were detected in 9 of 19 (47%) type 1 diabetic patients and 16 of 22 (73%) nondiabetic siblings, consistent with this region having immunostimulatory properties. The study reports for the first time T-cell lines reactive to IA-2 from diabetic patients and defines an immunodominant region of the molecule.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens, http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, http://linkedlifedata.com/resource/pubmed/chemical/HLA Antigens, http://linkedlifedata.com/resource/pubmed/chemical/Immunodominant Epitopes, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/PTPRN protein, human, http://linkedlifedata.com/resource/pubmed/chemical/PTPRN2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments, http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatase..., http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases, http://linkedlifedata.com/resource/pubmed/chemical/Receptor-Like Protein Tyrosine...
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
356-66
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10868956-Adolescent, pubmed-meshheading:10868956-Autoantigens, pubmed-meshheading:10868956-Cell Line, pubmed-meshheading:10868956-Child, pubmed-meshheading:10868956-Child, Preschool, pubmed-meshheading:10868956-Cytoplasm, pubmed-meshheading:10868956-Diabetes Mellitus, Type 1, pubmed-meshheading:10868956-Epitopes, pubmed-meshheading:10868956-Female, pubmed-meshheading:10868956-HLA Antigens, pubmed-meshheading:10868956-Humans, pubmed-meshheading:10868956-Immunodominant Epitopes, pubmed-meshheading:10868956-Infant, pubmed-meshheading:10868956-Male, pubmed-meshheading:10868956-Membrane Glycoproteins, pubmed-meshheading:10868956-Membrane Proteins, pubmed-meshheading:10868956-Peptide Fragments, pubmed-meshheading:10868956-Protein Tyrosine Phosphatase, Non-Receptor Type 1, pubmed-meshheading:10868956-Protein Tyrosine Phosphatases, pubmed-meshheading:10868956-Receptor-Like Protein Tyrosine Phosphatases, Class 8, pubmed-meshheading:10868956-T-Lymphocytes
pubmed:year
2000
pubmed:articleTitle
T-cell lines reactive to an immunodominant epitope of the tyrosine phosphatase-like autoantigen IA-2 in type 1 diabetes.
pubmed:affiliation
Department of Medicine, Guy's, King's College and St Thomas' School of Medicine, London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't