Autoimmune diseases may not stem from defects in the immune system alone. Rather, developmental genetic abnormalities in organ tissues may make those organs more susceptible to autoimmune disorders, according to a paper published online today in Immunology and Cell Biology.

"The former explanations of how these [autoimmune] diseases occur weren't totally satisfactory," Denise Faustman of Harvard Medical School, lead author of the study, told The Scientist. "Obviously the immune system plays a role, but maybe we should think about the target tissue more."

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. She 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.

In a commentary accompanying the paper, Adrian Liston, senior fellow at the University of Washington, warned that the findings require further investigation, especially into what pathological consequences arise in the defected organs as autoimmune diseases develop. He wrote that while Hox11 expression in organs with defects seems to correlate with autoimmunity, "the literature abounds with NOD defects which ended up being unrelated to their susceptibility to autoimmunity."