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March 14, 2001 Search
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Innate and Adaptive Immune Responses in Children With
Regression Autism:
Evaluation of the Effects of Environmental Factors
Including Vaccination
Journal of Allergy and Clinical Immunology
February 2001, part 2 • Volume 107 • Number 2
[The website address for this abstract has not yet been
provided to the FEAT Daily Newsletter.
To inquire for this information as it becomes available, contact the
editor at editor@feat.org. The full text of the research study is also
being pursued. Any reader who has
online access to the Journal of Allergy and Clinical Immunology is asked to
provide us with a copy of the paper for our study, at the same address. -ls ]
Harumi Jyonouchi; Sining Sun; Hoa Le
University of Minnesota,
Minneapolis, MN
Etiology of autism is unknown. However, there appears to
be a casual association between onset of regression/autistic behavior and
infant immunization/viral infection/adverse reactions to common food antigens (gluten
and cow’s milk). Previous literature
indicates the presence of autoantibodies against neuronal cells in autistic
children and subtle immune abnormalities such as skewed T2 responses.
In this study, we hypothesized that children with
regression autism may have aberrant immune responses against these common,
usually benign environmental factors, resulting in inflammatory and/or
autoimmune conditions in the CNS. As a first step to examine our hypothesis, we
determined innate and adaptive immune responses in children with autism spectrum
disorders (N=35, Age 2-14 yrs, median: 6 yr, 24 males and 9 females).
Innate immune responses are assessed by measuring
production of TNF-, IL-1, IL-6, sTNFRI, and sTNFRII after incubating peripheral
blood mononuclear (PBMN) cells overnight with endotoxin (LPS: 0.1 to 10 µg/ml). Adaptive immune responses are assessed by
measuring T cell cytokine (IFN-, IL-4, IL-5 and IL-10) production in response
to recall antigens (tetanus and dust mite), mitogens (PHA and Con A) and IFN-
inducing cytokines (IL-12p70 and IL-18) after culturing cells for 4 days with
these stimuli. Production of IL-12p40, IL-18, and TGF- was also measured in
this setting.
Controls were obtained from healthy normal children (N=17,
Age 2-16 yrs, median: 11 yrs). Onset of autism/developmental regression with immunization
was reported in 27/35 patients and 32/35 patients were reported to have
improvement of behavior by parents/teachers/therapists with a casein-free/gluten-free
diet. Autistic children produced higher TNF-(p<0.01), sTNFRII (p=0.038), and
IL-6 (p=0.01) with a low dose of LPS (0.1 µg/ml) than controls.
This is due to the presence of a subset of patients who
produced large amounts of these cytokines. In fact, 27/35 (77.1%) study subjects
produced higher than the maximum levels of TNF-, sTNFRII, IL-6 and/or IL-1
observed in controls with a low dose of LPS. We also observed elevated serum
levels of these cytokines in 8/18 autistic children.
Our results thus indicate a high frequency of excessive
innate immune responses in children with regression autism. These results may
partly explain apparent association between onset of regression/autistic
behavior and immunization in these children. Production of IFN-, IL-5, IL-10
and IL-12p40 was highly variable in autistic children. IL-4, IL-18, and TGF-production
by PBMN cells were generally low and did not differ between the study subjects
and controls.
We also assessed T1/T2 responses by comparing the ratio of
IFN-/IL-5 levels produced with recall antigens. The ratio of IFN-/IL-5 did not
differ between autistic children and controls. However, 7 and 8 out of 35
autistic children produced significantly high IL-12p40 with recall antigens and
IL-12/IL-18, respectively. IL-10 production was markedly variable in autistic
children: 10 and 11 out of 35 subjects produced high amounts of IL-10 with PHA
and tetanus, respectively, while 12/35 subjects produced significantly low
IL-10 with PHA as compared to controls.
These results also indicate aberrant production of
regulatory cytokines for T cell responses in subsets of autistic children.
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