The study included data on 3,325 Danish children diagnosed with autism spectrum disorder who were born in Denmark from 1993 to 2004. Of these, 1,089 were diagnosed with infantile autism.

Dr. William W. Eaton, chairman of the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University, and his team found that many of these children also mothers with a family history of autoimmune diseases. Autoimmune diseases, such as RA develop when antibodies that normally fight infectious organisms instead attack the body itself.

In addition, the team found that children with a family history of type 1 diabetes have an increased risk of infantile autism.

Previous studies have found a connection between autism and a maternal history of type 1 diabetes and rheumatoid arthritis. However, this is the first study to document a link between autism and celiac disease, according to the study’s authors.

The researchers say their study leaves many questions unanswered. But they say it’s possible babies are affected by their mother’s antibodies while in the womb. Their mother’s disease also may create an abnormal environment.

Autism affects roughly 1 in 150 children by age 8. The symptoms include impaired communication and socializing skills, rigid routines and repetitive behaviors. Known risk factors include family history, fathers older than 40, being male, and diseases such as tuberous sclerosis, Tourette’s syndrome, epilepsy and Fragile X syndrome.

The results of the study were published in the online journal Pediatrics.

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Originally posted 2009-07-24 12:15:57. Republished by Blog Post Promoter

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To perform their analysis, the research team from the Karolinska Institute and Stockholm accessed information from national registers to conduct a case controlled study or people born between 1973 and 2002.

The research involved 333 cases of RA that were diagnosed in patients that were between the ages of 16 and 29 years and 3,334 cases of juvenile idiopathic arthritis (JIA). They matched each of these cases with 4 control subjects based on gender and age.

The researchers found that people who had a serious infection in their first year had twice the risk of developing JIA. They also found that babies that were premature, small or had a low birth weight demonstrated a reduced risk for RA, although they don’t know why.

In addition, they found that having a high birth weight or having more than 3 older siblings does not have a significant impact of risk of developing RA.

Said lead author Dr. Cecilia Carlens concludes, “Nobody had thought of this relationship with early-in-life infections and how they can affect the immune system.

“Our results indicate that infections during the first year of life and possibly also factors related to size at and timing of birth may be of etiological importance in the pathogenesis of RA and JIA.”

The results of the study were published in the Tuesday edition of the online journal Annals of the Rheumatic Diseases.

Originally posted 2008-10-31 12:00:01. Republished by Blog Post Promoter

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A new study conducted by researchers at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge has resulted in a breakthrough in the understanding of how autoimmune responses can be controlled.

In a normal immune system, the body develops immune cells to recognize foreign material, like bacteria. Once encountered, the immune cells respond to eliminate the foreign material. Any rogue immune cells that would attack the body itself are destroyed during development or are regulated by special cell. A key gene in these regulatory cells is called Foxp3. Those people that either lack the Foxp3 gene or have a mutated version of the gene have dysfunctional immune regulation which can result in autoimmune diseases.

As a part of the study, scientists created a genetically engineered form of Foxp3 that can change developing immune cells into regulatory cells that have the ability to suppress immune response. They then injected the engineered gene into animals that were missing the Foxp3 gene.

Said group leader Dr. Alexander Betz: “When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process.”

The scientists are now working on determining the molecular mechanisms involved in the functioning of the Foxp3 gene and applying that to human cells. In that research they need to ensure that the human form of the gene does not negatively impact the body’s immune system.

“If Foxp3 functions as a key developmental switch in human immune cells, there is potential for a new avenue of therapy development that could transform arthritis treatment” — Dr. Betz.

The study was published in the current issue of the journal PLoS Biology.

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