Table 3.
Immune alterations in ASD patients and links to microbiota and GI abnormalities.
| Subject | Behavior | Description | Microbiota | Immune | GI | Reference(s) |
|---|---|---|---|---|---|---|
|
human (3–28 yo) |
autism | 46% (n=28/61) of ASD patients had family members with autoimmune disorders; immediate relatives with autoimmune disorders increased prevalence of autism diagnosis from 4 to 21%; autoimmune disorders include type 1 diabetes, rheumatoid arthritis, hypothyroidism, and system lupus erythematosus. |
X | (137) | ||
|
children (1–17 yo) |
autism, Asperger’s | LPS stimulated innate immune reaction that was stronger in ASD individuals (n=71), leading to elevated TNF-α, IL- 1β and IL-6 production. |
X | X | (63, 138) | |
| human (5–44 yo) | autism | Postmortem brain show increased microglia and astroglia activation. Brain and CSF showed increased proinflammatory cytokines. |
X | (16) | ||
|
children (5.9 ± 3.9 yo) |
autism | ASD (n=37) patients compared to control (n=29) had elevated sera IgG and IgM BDNF levels. |
X | (139) | ||
|
children (4–15 yo) |
autism, Asperger’s | ASD with GI (n= 18) compared to control (n=27) had enhanced pro- inflammatory cytokine profile, increased TNFα, INFγ, IL-4, and IL-5, decreased regulatory cytokine IL-10. |
X | X | (140) | |
|
children (42 ± 9.8 mo) |
autism, early onset, regressive |
ASD (n=116), contol (n= 96), developmental delays (n=32), ASD had decreased levels of IgG and IgM subclass. |
X | (141) | ||
| ASD mothers | autism | Maternal antibodies for fetal brain proteins were elevated in mothers of ASD children. ASD mothers (n=61), typical mothers (n=62), developmental delay mothers (n=40). |
X | (142) | ||
|
children (avg 3.47 yo) |
autism | ASD (n=114), contol (n= 96), developmental delays (n=31), ASD had increased levels of IgG4 subclass. |
X | (143) | ||
|
children (avg 3.2 yo) |
autism | ASD patients had elevated autoantibodies in plasma that were directed to cerebellar protein extracts. |
X | (144, 145) |
||
| children (>1 yo) | autism, Asperger | 3325 diagnosed children with ASD in Denmark had increased risk of ASD diagnosis when they had a family history of type 1 diabetes and rheumatoid arthritis. |
X | (131) | ||
| adult (18–44 yo) | severe autism | ASD patients (n=22) had elevated levels of serum endotoxin that were correlated with decreased VABX socialization scores and trend towards increase in proinflammatory cytokines IL-1β and IL-6, but not significant. |
X | X | (21) | |
|
children (median 3.6 yo) |
lethargy, stereotypy, hyperactivity, impaired communication/so cialization |
Elevated brain and CSF chemokine (MCP-1, RANTES, and eotaxin) in ASD patients (n=80) was associated with higher aberrant behavior and impaired learning and social skills. |
X | (146) | ||
|
children (median 3.4 yo) |
non-regressive and regressive autism |
ASD children (n=97) showed higher plasma levels of IL-6 and IL-12p40. |
X | (147) | ||
|
children (7–15 yo) |
high functioning autism |
Increased levels of serum IL-17 in male subjects with high functioning ASD (n=28). |
X | (64) | ||
|
children (5–17 yo) |
Regressive autism | ASD children (n=34) had decreased levels of plasma IL-23, but no changes in IL-17. |
X | (148, 149) |
||
|
children (24–60 mo) |
autism | Increased production of IL −17 and IL-13 in co-morbid autism (n=45) and asthma children (n=12). |
X | (150) |