Linked Life Data

10593564

Source:http://linkedlifedata.com/resource/pubmed/id/10593564

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-1-11
pubmed:abstractText
Diabetes prone (DP) BB rats develop spontaneous autoimmune hyperglycemia. Coisogenic diabetes resistant (DR) BB rats develop diabetes in response to immunological and environmental perturbants, but not spontaneously. Both are used to model human insulin-dependent diabetes mellitus (IDDM). Deficiencies in natural killer (NK) T cells have been implicated in the expression of human IDDM, but little is known of their phenotype or function in the rat. We now report that the phenotype of NK T cells in the rat is alphabetaTcR+ CD8+ CD4-, comparable to the NK T cell phenotype reported for humans, which is alphabetaTcR+ CD4- Valpha24-JalphaQ, and either CD8- or CD8alphaalpha+. We also report that DP- but not DR-BB rats are severely deficient in splenic and intrahepatic NKR-P1+ alphabetaTcR+ (NK T) cells. Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen. We observed that the majority of rat NK T cells express RT6+. In addition, injection of cytotoxic anti-RT6.1 monoclonal antibody depleted splenic and intrahepatic RT6+ NK T cells, T cells, and NK cells, but left intact the RT6- subset of each population. These results suggest that deficiencies in NK T cells may play a role in the susceptibility of DP- and DR-BB rats, respectively, to spontaneous and induced autoimmune IDDM.
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
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-14
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10593564-ADP Ribose Transferases, pubmed-meshheading:10593564-Animals, pubmed-meshheading:10593564-Antibodies, Monoclonal, pubmed-meshheading:10593564-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:10593564-Diabetes Mellitus, Type 1, pubmed-meshheading:10593564-GPI-Linked Proteins, pubmed-meshheading:10593564-Histocompatibility Antigens, pubmed-meshheading:10593564-Immunophenotyping, pubmed-meshheading:10593564-Killer Cells, Natural, pubmed-meshheading:10593564-Liver, pubmed-meshheading:10593564-Membrane Glycoproteins, pubmed-meshheading:10593564-Rats, pubmed-meshheading:10593564-Rats, Inbred BB, pubmed-meshheading:10593564-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:10593564-Spleen, pubmed-meshheading:10593564-T-Lymphocyte Subsets, pubmed-meshheading:10593564-Thymus Gland
pubmed:year
1999
pubmed:articleTitle
Diabetes prone BB rats are severely deficient in natural killer T cells.
pubmed:affiliation
Department of Medicine, University of Massachusetts Medical School, Worcester 01655, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't