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Diabetes: Compound Stops Islet Destruction

 
  September, 5 2001 19:27
your information resource in human molecular genetics
 
     
Type I diabetes, in which the beta cells of the pancreas produce too little or no insulin, accounts for 3% of all new cases of diabetes each year. While the routine treatment for this disease is injections of insulin, an international team of scientists may have discovered a potentially new therapy for the condition (Nature Medicine, Vol. 7, No. 9, Sep 01).

One feature of Type 1 diabetes is a decrease in the number of Natural Killer T (NKT) cells of the immune system. This deficit also occurs in a mouse model of diabetes known as the NOD, or non-obese diabetic mouse model. The compound alpha-galactosylceramide (a-GalCer), binds to receptors on NKT-cells called CD1d receptors, and stimulates the production of cytokines from NKT-cells.

When they administered a-GalCer to NOD mice, the scientists found that it protected mice from developing diabetes even when given after onset of insulitis, and prolonged the survival of insulin-producing pancreatic islets transplanted into newly diabetic mice. In addition, a-GalCer enhanced the response to, and production of, vital cytokines by NKT cells.

The authors propose that a-GalCer decreases the destruction of islet cells by the body's own immune system and may have beneficial effects in diabetic patients.

Contact:

Dr. Terry Delovitch
Department of Microbiology and Immunology
University of Western Ontario
London, Ontario, Canada
Tel: +1 519-663-3972
Fax: +1 519-663-3847
Email: del@rri.on.ca

Dr. Jean-François Bach
Institut National de la Santé
Centre de l'Association Claude Bernard
Hôpital Necker
61 rue de Sèvres
Paris Cedex 15, France
Tel: +33 1 444 9 5371
Fax: +33 1 4306 2388
E-mail: bach@necker.fr


Dr. Luc Van Kaer
Howard Hughes Medical Institute
Department of Microbiology and Immunology
Vanderbilt University School of Medicine
Nashville, Tennessee
Tel: +1 615 343 2707
Fax: +1 615 343 2972
Email: vankael@ctrvax.vanderbilt.edu

(C) Nature Medicine press release.


Message posted by: Trevor M. D'Souza

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