Evidence map›Paper›PMID 28180029›Full record

ArticleJournal of clinical & cellular immunology2016

The Major Histocompatibility Complex (MHC) in Schizophrenia: A Review.

Ryan Mokhtari, Herbert M Lachman

Open access · greenAbstract read
In one paragraph

Article in Journal of clinical & cellular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 5 pooled it
3.4field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 5 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Mapping the genetic landscape of suicide risk: Insights from genomic SEM.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

2 authors at 1 institution in 1 country.

Ryan MokhtariDepartment of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, New York, USA.
Herbert M LachmanDepartment of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, New York, USA; Department of Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, New York, USA; Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, New York, USA; Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, New York, USA.
Albert Einstein College of Medicine · US

Funding

Monoallelic expression in neurons derived from induced pluripotent stem cellsR01MH099427 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI LACHMAN, HERBERT M · 2013 to 2017
$2.1M
NIMH NIH HHS R01 MH099427
6 · The paper itself

Abstract

Epidemiological studies and mouse models suggest that maternal immune activation, induced clinically through prenatal exposure to one of several infectious diseases, is a risk factor in the development of schizophrenia. This is supported by the strong genetic association established by genome wide association studies (GWAS) between the human leukocyte antigen (HLA) locus and schizophrenia. HLA proteins (also known in mice as the major histocompatibility complex; MHC) are mediators of the T-lymphocyte responses, and genetic variability is well-established as a risk factor for autoimmune diseases and susceptibility to infectious diseases. Taken together, the findings strongly suggest that schizophrenia risk in a subgroup of patients is caused by an infectious disease, and/or an autoimmune phenomenon. However, this view may be overly simplistic. First, MHC proteins have a non-immune effect on synaptogenesis by modulating synaptic pruning by microglia and other mechanisms, suggesting that genetic variability could be compromising this physiological process. Second, some GWAS signals in the HLA locus map near non-HLA genes, such as the histone gene cluster. On the other hand, recent GWAS data show association signals near B-lymphocyte enhancers, which lend support for an infectious disease etiology. Thus, although the genetic findings implicating the HLA locus are very robust, how genetic variability in this region leads to schizophrenia remains to be elucidated.

Indexed as

MHCSchizophrenia

Identifiers

PMID28180029
PMCPMC5293234
OpenAlexW2568419125

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.