Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-3-30
pubmed:abstractText
Type 1 diabetes can be inhibited in standard NOD mice by autoantigen-specific immunotherapy targeting pathogenic CD8+ T-cells. NOD.?2m(null).HHD mice expressing human HLA-A2.1 but lacking murine major histocompatibility complex class I molecules develop diabetes characterized by CD8 T-cells recognizing certain autoantigenic peptides also targeted in human patients. These include peptides derived from the pancreatic ?-cell proteins insulin (INS1/2 A(2-10) and INS1 B(5-14)) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP(265-273) and IGRP(228-236)). Hence, NOD.?2m(null).HHD mice represent a model system for developing potentially clinically translatable interventions for suppressing diabetogenic HLA-A2.1-restricted T-cell responses.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1939-327X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1229-36
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Prevention of "Humanized" diabetogenic CD8 T-cell responses in HLA-transgenic NOD mice by a multipeptide coupled-cell approach.
pubmed:affiliation
Jackson Laboratory, Bar Harbor, Maine, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural