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Autism and Immune Dysfunction

Posted Oct 01 2008 8:03pm

CHILDREN WITH AUTISM HAVE DISTINCTLY DIFFERENT IMMUNE SYSTEM REACTIONS COMPARED TO TYPICAL CHILDREN
Immunologists from UC Davis M.I.N.D. Institute find clear biological component to perplexing childhood neurological disorder
May 5, 2005


(BOSTON, Mass.) – A new study by researchers at the University of California, Davis, M.I.N.D. Institute and the NIEHS Center for Children’s Environmental Health demonstrate that children with autism have different immune system responses than children who do not have the disorder. This is important evidence that autism, currently defined primarily by distinct behaviors, may potentially be defined by distinct biologic changes as well.

The study was released at the 4th International Meeting for Autism Research (IMFAR) – a meeting of autism scientists started by Cure Autism Now, the UC Davis M.I.N.D. Institute and the National Alliance for Autism Research to accelerate knowledge of this increasingly common and perplexing disorder. It is estimated that autism now affects 1 in every 166 children.

“Understanding the biology of autism is crucial to developing better ways to diagnose and treat it,” said Judy Van de Water, associate professor of rheumatology, allergy and clinical immunology at the UC Davis School of Medicine and the UC Davis M.I.N.D. Institute. “While impaired communication and social skills are the hallmarks of the disorder, there has not yet been strong scientific evidence that the immune system is implicated as well. We now need to design carefully controlled studies that tell us even more about the way in which a dysfunctional immune system may or may not play a role in the disorder itself.”

Van de Water, along with co-investigator of the study Paul Ashwood, assistant professor of medical microbiology and immunology at the UC Davis M.I.N.D. Institute, isolated immune cells from blood samples taken from 30 children with autism and 26 typically developing children aged between two and five years of age. The cells from both groups were then exposed to bacterial and viral agents that usually provoke T-cells, B cells and macrophages – primary players in the immune system.

Of the agents tested in the study - tetanus toxoid, lippopolysaccharide derived from E. coli cell walls, a plant lectin known as PHA, and a preparation of the measles, mumps and rubella vaccine antigens - the researchers found clear differences in cellular responses between patients and controls following exposure to the bacterial agents and PHA.

In response to bacteria, the researchers saw lower levels of protein molecules called cytokines in the group with autism. Cytokines function as mediators of the immune response, carrying messages between B, T and other immune cells. They also are known to be capable of having profound effects on the central nervous system, including sleep and the fever response. Immune system responses to PHA, in contrast, produced more varied cytokine levels: Higher levels of certain cytokines and lower levels of others.

According to Van de Water and Ashwood, these studies illustrate that under similar circumstances, the cytokine responses elicited by the T-cells, B-cells, and macrophage cell populations following their activation differs markedly in children with autism compared to age-matched children in the general population. Cytokines are known to affect mood and behavior, and while their specific role in the development of autism remains unclear, the potential connection is an intriguing area of research that warrants further investigation.

"This study is part of a larger effort to learn how changes in immune system response may make some children more susceptible to the harmful effects of environmental agents," said Kenneth Olden, director of the National Institute of Environmental Health Sciences, the federal agency that provided funding for the study. "A better understanding of the connection between altered immune response and autism may lead to significant advances in the early detection, prevention and treatment of this complex neurological disorder."

"We would like to take these findings and explore whether, for example, the cytokine differences are specific to certain subsets of patients with autism, such as those with early onset, or those who exhibit signs of autism later during development," Ashwood said. He added that the logical next step is to look directly at specific cell populations that may be responsible for the diverging responses between patients and controls.

This study was supported by grants from the National Institutes of Environmental Health Sciences, the U.S. Environmental Protection Agency, the UC Davis M.I.N.D. Institute, Ted Lindsay Foundation and Visceral. The UC Davis M.I.N.D. (Medical Investigation of Neurodevelopmental Disorders) Institute is a unique collaborative center for research into the causes and treatments of autism, bringing together parents, scientists, clinicians and educators. For further information, go to http://www.ucdmc.ucdavis.edu/mindinstitute.

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