Evidence map›Paper›PMID 36300375›Full record

ReviewBioscience reports2022

Systemic maternal inflammation promotes ASD via IL-6 and IFN-γ.

Daniel Majerczyk, Elizabeth G Ayad, Kari L Brewton, Pichrasmei Saing, Peter C Hart

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Brain, behavior, & immunity - health · 2026
    Article
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  5. The Eph-ephrin system in neuropsychiatric and neurodevelopmental disorders.Journal of psychiatry & neuroscience : JPN · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Daniel MajerczykCollege of Science, Health and Pharmacy, Roosevelt University, Illinois 60173, U.S.A.ORCID 0000-0003-0096-526X
Elizabeth G AyadCollege of Science, Health and Pharmacy, Roosevelt University, Illinois 60173, U.S.A.
Kari L BrewtonCollege of Science, Health and Pharmacy, Roosevelt University, Illinois 60173, U.S.A.
Pichrasmei SaingCollege of Science, Health and Pharmacy, Roosevelt University, Illinois 60173, U.S.A.
Peter C HartCollege of Science, Health and Pharmacy, Roosevelt University, Illinois 60173, U.S.A.ORCID 0000-0003-1843-9102
Roosevelt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurological disorder that manifests during early development, impacting individuals through their ways of communicating, social behaviors, and their ability to perform day-to-day activities. There have been different proposed mechanisms on how ASD precipitates within a patient, one of which being the impact cytokines have on fetal development once a mother's immune system has been activated (referred to as maternal immune activation, MIA). The occurrence of ASD has long been associated with elevated levels of several cytokines, including interleukin-6 (IL-6) and interferon gamma (IFN-γ). These proinflammatory cytokines can achieve high systemic levels in response to immune activating pathogens from various extrinsic sources. Transfer of cytokines such as IL-6 across the placental barrier allows accumulation in the fetus, potentially inducing neuroinflammation and consequently altering neurodevelopmental processes. Individuals who have been later diagnosed with ASD have been observed to have elevated levels of IL-6 and other proinflammatory cytokines during gestation. Moreover, the outcome of MIA has been associated with neurological effects such as impaired social interaction and an increase in repetitive behavior in animal models, supporting a mechanistic link between gestational inflammation and development of ASD-like characteristics. The present review attempts to provide a concise overview of the available preclinical and clinical data that suggest cross-talk between IL-6 and IFN-γ through both extrinsic and intrinsic factors as a central mechanism of MIA that may promote the development of ASD.

Indexed as

Autism Spectrum DisorderPrenatal Exposure Delayed EffectsAnimalsCytokinesFemaleHumansInflammationInterferon-gammaInterleukin-6PlacentaPregnancyCytokinesInterferon-gammaInterleukin-6ASDautism-spectrum disordersinterferon-gammainterleukin 6maternal immune activationMIA

Identifiers

PMID36300375
PMCPMC9670245
OpenAlexW4307427049

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.