Evidence map›Paper›PMID 28688579›Full record

ArticleBiological psychiatry2018

Replicable and Coupled Changes in Innate and Adaptive Immune Gene Expression in Two Case-Control Studies of Blood Microarrays in Major Depressive Disorder.

Gwenaël G R Leday, Petra E Vértes, Sylvia Richardson, Jonathan R Greene, Tim Regan, Shahid Khan, Robbie Henderson, Tom C Freeman, Carmine M Pariante, Neil A Harrison and 5 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06182722 (Association of Peripheral Immune Cells With Antidepressant Treatment Response), which is not on this map. Cited by 141 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 3 pooled it
6.4field-weighted citation impact, top 2% 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.

NCT06182722 unknown statusnot on this mapstarted 2024, after this paper: background citation

Association of Peripheral Immune Cells With Antidepressant Treatment Response

Typeobservational_patient_registrySponsorShanghai Mental Health CenterRan2024 to 2025Enrolled90ConditionsDepressive Disorder, Genetic ChangeArmsMental assessments
3 · Its place in the literature

Who cites it

141 citing papers in PubMed, 3 syntheses or guidelines pooled it, 222 citations in OpenAlex.

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81 more citing papers are in PubMed but not listed here.

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

15 authors at 11 institutions in 2 countries.

Gwenaël G R LedayMedical Research Council Biostatistics Unit, Cambridge, United Kingdom.
Petra E VértesDepartment of Psychiatry, University of Cambridge, Cambridge, United Kingdom.
Sylvia RichardsonMedical Research Council Biostatistics Unit, Cambridge, United Kingdom.
Jonathan R GreeneRancho BioSciences, San Diego, California.
Tim ReganRoslin Institute, University of Edinburgh, Edinburgh, United Kingdom.
Shahid KhanImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom.
Robbie HendersonImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom.
Tom C FreemanRoslin Institute, University of Edinburgh, Edinburgh, United Kingdom.
Carmine M ParianteInstitute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Neil A HarrisonBrighton and Sussex Medical School, University of Sussex, Brighton, United Kingdom.
MRC Immunopsychiatry Consortium
V Hugh PerryCentre for Biological Sciences, University of Southampton, Southampton, United Kingdom.
Wayne C DrevetsJanssen Research & Development, Titusville, New Jersey.
Gayle M WittenbergJanssen Research & Development, Titusville, New Jersey.
Edward T BullmoreDepartment of Psychiatry, University of Cambridge, Cambridge, United Kingdom; Cambridgeshire and Peterborough National Health Service Foundation Trust, Cambridge, United Kingdom; ImmunoPsychiatry, GlaxoSmithKline Research & Development, Stevenage, United Kingdom. Electronic address: etb23@cam.ac.uk.
GlaxoSmithKline (United Kingdom) · GBJanssen (United States) · USMedical Research Council · GBRoslin Institute · GBBrighton and Sussex Medical School · GBCambridgeshire and Peterborough NHS Foundation Trust · GBKing's College London · GBUniversity of Cambridge · GBNational Health Service · GBRancho BioSciences (United States) · USUniversity of Southampton · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F003722/1Biotechnology and Biological Sciences Research Council BB/I001107/1Biotechnology and Biological Sciences Research Council BBS/E/D/20211551Biotechnology and Biological Sciences Research Council BBS/E/D/20211552Biotechnology and Biological Sciences Research Council BBS/E/D/20211553Biotechnology and Biological Sciences Research Council BBS/E/D/20211554Medical Research Council G108/603Medical Research Council MC_UP_0801/1Medical Research Council MC_UU_00002/10Medical Research Council MR/K020706/1Medical Research Council MR/L014815/1Medical Research Council MR/N029488/1
6 · The paper itself

Abstract

backgroundPeripheral inflammation is often associated with major depressive disorder (MDD), and immunological biomarkers of depression remain a focus of investigation.

methodsWe used microarray data on whole blood from two independent case-control studies of MDD: the GlaxoSmithKline-High-Throughput Disease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control subjects) and the Janssen-Brain Resource Company study (94 patients and 100 control subjects). Genome-wide differential gene expression analysis (18,863 probes) resulted in a p value for each gene in each study. A Bayesian method identified the largest p-value threshold (q = .025) associated with twice the number of genes differentially expressed in both studies compared with the number of coincidental case-control differences expected by chance.

resultsA total of 165 genes were differentially expressed in both studies with concordant direction of fold change. The 90 genes overexpressed (or UP genes) in MDD were significantly enriched for immune response to infection, were concentrated in a module of the gene coexpression network associated with innate immunity, and included clusters of genes with correlated expression in monocytes, monocyte-derived dendritic cells, and neutrophils. In contrast, the 75 genes underexpressed (or DOWN genes) in MDD were associated with the adaptive immune response and included clusters of genes with correlated expression in T cells, natural killer cells, and erythroblasts. Consistently, the MDD patients with overexpression of UP genes also had underexpression of DOWN genes (correlation > .70 in both studies).

conclusionsMDD was replicably associated with proinflammatory activation of the peripheral innate immune system, coupled with relative inactivation of the adaptive immune system, indicating the potential of transcriptional biomarkers for immunological stratification of patients with depression.

Indexed as

Immunity, InnateBiomarkersCase-Control StudiesGene ExpressionGene Expression RegulationHumansMajor Depressive DisorderMicroarray AnalysisTranscriptomeWernicke EncephalopathyBiomarkersAffymetrixBayesianBiomarkerInflammationSystemsTranscriptome

Identifiers

PMID28688579
PMCPMC5720346
OpenAlexW2731772132

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Registered trials

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.