Source:http://linkedlifedata.com/resource/pubmed/id/17327430
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
2007-2-28
|
| pubmed:abstractText |
Monoclonal antibodies to T-cell coreceptors have been shown to tolerise autoreactive T-cells and prevent or even reverse autoimmune pathology. In type 1 diabetes, there is a loss of insulin-secreting beta-cells, and a cure for type 1 diabetes would require not only tolerance induction but also recovery of the functional beta-cell mass. Although we have previously shown that diabetic mice have increased numbers of ductal progenitors in the pancreas, there is no evidence of any increase of insulin-secreting cells in the ducts. In contrast, in the adult human pancreas of patients with chronic pancreatitis, we can demonstrate, in the ducts, increased numbers of insulin-containing cells, as well as cells containing other endocrine and exocrine markers. There are also significantly increased numbers of cells expressing the homeodomain protein, pancreatic duodenal homeobox-1. Anti-CD3 has been shown to reverse overt diabetes in NOD mice; thus, we have used this model to ask whether monoclonal antibody-mediated inhibition of ongoing beta-cell destruction enables islet regeneration to occur. We find no evidence that such monoclonal antibody therapy results in either regeneration of insulin-secreting beta-cells or of increased proliferation of islet beta-cells.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0012-1797
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
56
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
634-40
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:17327430-Adolescent,
pubmed-meshheading:17327430-Adult,
pubmed-meshheading:17327430-Animals,
pubmed-meshheading:17327430-Antibodies, Monoclonal,
pubmed-meshheading:17327430-Antigens, CD3,
pubmed-meshheading:17327430-Child,
pubmed-meshheading:17327430-Child, Preschool,
pubmed-meshheading:17327430-Diabetes Mellitus,
pubmed-meshheading:17327430-Female,
pubmed-meshheading:17327430-Glucagon,
pubmed-meshheading:17327430-Humans,
pubmed-meshheading:17327430-Insulin,
pubmed-meshheading:17327430-Islets of Langerhans,
pubmed-meshheading:17327430-Male,
pubmed-meshheading:17327430-Mice,
pubmed-meshheading:17327430-Mice, Inbred NOD,
pubmed-meshheading:17327430-Middle Aged,
pubmed-meshheading:17327430-Pancreas,
pubmed-meshheading:17327430-Pancreatitis, Chronic,
pubmed-meshheading:17327430-Regeneration
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
Patients with chronic pancreatitis have islet progenitor cells in their ducts, but reversal of overt diabetes in NOD mice by anti-CD3 shows no evidence for islet regeneration.
|
| pubmed:affiliation |
Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB21QP, U.K.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|