Stem Cell Therapy Prevents Diabetes Type 1 In Mice

NEW YORK (Reuters Health) - Introduction of stem cells expressing diabetes resistant alleles led to diabetes type 1 resistance in mice susceptible to the condition, researchers report in the October issue of the Journal of Clinical Investigation.

Dr. John Iacomini of Harvard Medical School, Boston and colleagues used retroviral transduction of autologous bone marrow hematopoietic stem cells, which expressed diabetes-resistant MHC class II alleles, to treat NOD mice, animals that spontaneously develop diabetes type 1.

This prevented the development of self-reactive diabetogenic T cells and protected the mice from insulinitis and destruction of beta cells in the pancreas.

Dr. Iacomini told Reuters Health: “In proof-of-principle experiments we demonstrated it is possible that a gene therapy based approach can be used to overcome autoimmunity associated with type 1 diabetes by establishing a state of molecular chimerism.”

“If induction of molecular chimerism can be modified to make it acceptable for use in humans,” Dr. Iacomini continued, “it might prevent type 1 diabetes. In conjunction with islet transplantation, inducing molecular chimerism could also provide a cure for pre-existing type 1 diabetes.”

“Molecular chimerism,” he concluded, “could also be used to reshape the immune system to prevent transplant rejection, or treat other autoimmune diseases.”

In an accompanying editorial, Drs. Remi J. Creusot and C. Garrison Fathman of Stanford University School of Medicine, California, characterize the study as being among those “pioneering research toward reinstating central tolerance, possibly the most effective way to cure autoimmunity.”

Source: J Clin Invest 2004;114:969-978:892-894. [ Google search on this article ]

MeSH Headings:Animal Diseases: Biological Therapy: Disease Models, Animal: Genetic Engineering: Genetic Techniques: Investigative Techniques: Therapeutics: Gene Therapy: Analytical, Diagnostic and Therapeutic Techniques and Equipment: DiseasesCopyright © 2002 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

MORE ON THIS TOPIC