Linked Life Data

21592863

Source:http://linkedlifedata.com/resource/pubmed/id/21592863

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-6-14
pubmed:abstractText
Type 1 diabetes (T1D) is an autoimmune disease in both humans and the nonobese diabetic (NOD) mouse, in which the insulin-producing-cells of the pancreatic islets are destroyed by a beta islet cell-specific T cell immune response. We recently reported that interferon (IFN)-? is an early trigger of the T1D process in NOD mice. Here, we show that extensive blockade of IFN-? action by a monoclonal antibody specific to IFN-? receptor 1 results in nearly complete prevention of T1D in NOD mice. Whether professional IFN-? producing cells, plasmacytoid dendritic cells (pDCs), are responsible for the initiation of T1D has been unclear. Here we demonstrate that depletion of pDCs in NOD mice by a specific mAb given at 15-25 days of age significantly delays the onset and decreases the incidence of T1D. These findings indicate that pDC and pDC-derived IFN-? are the prime initiators of the pathogenesis of T1D in NOD mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1521-7035
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3-7
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
The role of interferon alpha in initiation of type I diabetes in the NOD mouse.
pubmed:affiliation
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't