An opinion piece in this Sunday's New York Times has shined a light on the important research being done on immune dysfunction and autism. The writer, Moises Velasquez-Manoff, author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases,” described autism as an inflammatory disease that begins during gestation. He noted many studies that link dysfunction in the immune system with autism spectrum disorder (ASD), citing Autism Speaks funded research. For example, the author refers to evidence that dysfunctions in the immune system and the response of the immune system may be important contributors to autism. This evidence stems from the work of Paul Patterson, Ph.D., of the California Institute of Technology. As we reported previously, when Dr. Patterson created artificial inflammation in pregnant mice, mimicking the response a mouse would have to a real infection, it caused behavioral problems that were similar to ASD in their offspring.
In addition, Velasquez-Manoff refers to the presence of autoantibodies (antibodies directed against one's own proteins) in mothers who have a child with autism. At the University of California, Davis, researchers are studying specific immune proteins and how they interact with the developing brain. Autism Speaks is currently funding a number of other studies that investigate the role of the immune system and whether individuals with ASD and immune problems may have different behavioral symptoms than those with ASD who don’t have immune issues.
While the immune system clearly plays an important role in ASD, researchers disagree on what the role is. Are these immune changes part of the cause of autism or a consequence of a poorly regulated immune system, or maybe both? It could be, as one study published last year showed, that abnormal brain development results in an immune response of its own.
As suggested by the New York Times article, science is already moving forward with some potential treatments, including the use of parasites to regulate the immune system. Right now, however, we do not know if any of the treatments mentioned are effective.
Autism Speaks has made substantial research investments in studying the role of immune function as a cause of autism, in helping to diagnose autism and in identifying treatments. The Autism Speaks community has voiced a great interest in further exploring the ways that immune dysfunction may contribute to the development or aggravation of autism symptoms.
“It is clear that research on the role of immune dysfunction in the underlying biology of autism, and the role for treatment targets, needs to be among the high priorities for autism research,” says Autism Speaks Chief Science Officer Geraldine Dawson, Ph.D.
The New York Times opinion piece also draws connections between the rising prevalence of autism and the rising prevalence of other immune disorders, including asthma and allergies. The author points to studies that relate these problems to the “modern day” immune system, which some researchers say is set in overdrive, partly because we live in a super-clean world with few parasites and other germs for our bodies to fight. Researchers are still investigating the extent to which this hypothesis may impact the immune system.
Please join Autism Speaks’ Facebook webchat with Dr. Patterson, who will field questions about the role of immune function in autism. Join the webchat on Wednesday, Aug. 29, at 3 p.m. ET, noon PT, and send advance questions to email@example.com. To join the live chat or sign up in advance for a reminder, go to Autism Speaks Facebook page.
This story was originally posted on Aug. 27 and updated on Aug. 28. To read the full New York Times opinion piece, click here. For a transcript of Dr. Patteron's webchat, click here. To read Autism Speaks’ prior news stories on research related to immune function, see this story on evidence that links immune function to autism, and this piece on the brain immune connection. You can explore research on immune function funded by Autism Speaks on our Grants search page.