|
 Children
with Autism Have Distinctly Different Immune System Reactions
Compared to Typical Children
UC Davis Health, June 6, 2005
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"Children
with autism have different immune system responses than children
who do not have the disorder, study shows."
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 - (BOSTON, Mass.)
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