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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1998-7-22
|
| pubmed:abstractText |
Type 1 (insulin-dependent) diabetes mellitus is strongly associated with autoimmune phenomena connected to the loss of beta-cells in the pancreatic islets. Despite considerable progress in our understanding of genetic susceptibility factors and islet autoimmunity preceding the clinical onset of Type 1 diabetes there are considerable gaps in our knowledge. First, the etiology is unclear. It is speculated that multiple etiological factors may initiate a common pathogenic pathway which results in immune-mediated beta-cell destruction. In 1998 we will need to learn more about the possible importance of gestational infections, as well as isolation of viral DNA or RNA from the blood of new-onset patients or marker-positive individuals. The scan of the whole genome has provided a smorgasbord of genetic regions which confer diabetes risk either alone or in combination. HLA remains the major genetic risk factor, and while HLA peptide binding information is considerable, we understand less of autoantigen processing and presentation. Cloned autoantigens and their use in standardized autoantibody assays have improved our ability to identify individuals at risk for diabetes. The diagnostic sensitivity and specificity of autoantibody markers for Type 1 diabetes are high as are their predictive values. We need methods to combine autoantibodies with genetic risk factors. The identification of individuals in different stages of their pathogenesis, including patients with so-called slowly progressive Type 1 diabetes (SPIDDM, LADA etc.), allow approaches to novel therapeutic interventions. Insulin is currently the therapeutic agent of choice and although spontaneous insulin-dependent diabetes in the NOD mouse and the BB rat can be prevented by immune suppression or modulation, this has not yet been possible in humans. The 1998 research on the interaction between environmental factors and susceptibility genes to initiate beta-cell specific autoreactivity should allow the development of therapies for prevention, and perhaps a cure, of insulin-dependent (Type 1) diabetes.
|
| pubmed:grant | |
| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0742-4221
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
14
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3-29
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading | |
| pubmed:year |
1998
|
| pubmed:articleTitle |
Immunology in diabetes: an update.
|
| pubmed:affiliation |
Department of Medicine, University of Washington, Seattle 98195-7710, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
|