Thursday, February 28, 2008

Embryonic defects cause diabetes

LONDON: Researchers have shown that autoimmune diseases, like Type 1 diabetes, may not stem from defects in the immune system alone, but also could be triggered by certain embryo defects.

Giving an alternative explanation as to what triggers diabetes, Denise Faustman at Harvard Medical School in Boston, US, and her colleagues found differences in the structure of several organs, including the pancreas, in mice predisposed to develop type 1 diabetes, even before any autoimmune attack takes place.

Faustman’s team suggested that this abnormal organ development before birth could predispose certain individuals to autoimmune disease.

The team observed before that mice and humans with type 1 diabetes are at a greater risk of developing hearing loss and Sjögren’s syndrome, an autoimmune disease affecting the salivary glands.

Faustman and her colleagues examined the organs of nonobese diabetic (NOD) mice that developed autoimmune symptoms of pancreatic and salivary gland destruction.

They found that these organs, while geographically far from each other, shared developmental abnormalities, and that their cell lineages all develop through the Hox11 transcription factor.

The team speculates that these organs are somehow predisposed to targeting by autoimmune diseases through their common lineage. Hox11 is expressed in normal mice but without organ defects.

“It challenges the orthodoxy that autoimmunity is solely caused by a defective immune system,” New Scientist magazine quoted Faustman, as saying.

The findings appear in the journal Immunology and Cell Biology .


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