Evidence map›Paper›PMID 27812316›Full record

ReviewFrontiers in neuroscience2016

Common Genetic Variants Found in HLA and KIR Immune Genes in Autism Spectrum Disorder.

Anthony R Torres, Thayne L Sweeten, Randall C Johnson, Dennis Odell, Jonna B Westover, Patricia Bray-Ward, David C Ward, Christopher J Davies, Aaron J Thomas, Lisa A Croen and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. The Role of Killer Ig-like Receptors in Diseases from A to Z.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Genetic relationship between the immune system and autism.Brain, behavior, & immunity - health · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Neuroinflammation in Autism Spectrum Disorders: Role of High Mobility Group Box 1 Protein.International journal of molecular and cellular medicine · 2017
    Review
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

11 authors at 3 institutions in 1 country.

Anthony R TorresCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
Thayne L SweetenBiology Department, Utah State University Brigham City, UT, USA.
Randall C JohnsonBSP CCR Genetics Core, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research Frederick, MD, USA.
Dennis OdellCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
Jonna B WestoverCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
Patricia Bray-WardCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
David C WardCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
Christopher J DaviesCenter for Integrated BioSystems, Utah State University Logan, UT, USA.
Aaron J ThomasDivision of Research, Kaiser Permanente of Northern California Oakland, CA, USA.
Lisa A CroenCenter for Integrated BioSystems, Utah State University Logan, UT, USA.
Michael BensonCenter for Persons with Disabilities, Utah State University Logan, UT, USA.
Utah State University · USFrederick National Laboratory for Cancer Research · USKaiser Permanente · US

Funding

CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

The "common variant-common disease" hypothesis was proposed to explain diseases with strong inheritance. This model suggests that a genetic disease is the result of the combination of several common genetic variants. Common genetic variants are described as a 5% frequency differential between diseased vs. matched control populations. This theory was recently supported by an epidemiology paper stating that about 50% of genetic risk for autism resides in common variants. However, rare variants, rather than common variants, have been found in numerous genome wide genetic studies and many have concluded that the "common variant-common disease" hypothesis is incorrect. One interpretation is that rare variants are major contributors to genetic diseases and autism involves the interaction of many rare variants, especially in the brain. It is obvious there is much yet to be learned about autism genetics. Evidence has been mounting over the years indicating immune involvement in autism, particularly the HLA genes on chromosome 6 and KIR genes on chromosome 19. These two large multigene complexes have important immune functions and have been shown to interact to eliminate unwanted virally infected and malignant cells. HLA proteins have important functions in antigen presentation in adaptive immunity and specific epitopes on HLA class I proteins act as cognate ligands for KIR receptors in innate immunity. Data suggests that HLA alleles and KIR activating genes/haplotypes are common variants in different autism populations. For example, class I allele (HLA-A2 and HLA-G 14 bp-indel) frequencies are significantly increased by more than 5% over control populations (

Indexed as

autismcommon genetic varianthaplotypeHLAKIR

Identifiers

PMID27812316
PMCPMC5071356
OpenAlexW2534442272

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.