Evidence map›Paper›PMID 25895500›Full record

ArticleJournal of neuroinflammation2015

Association of brain immune genes with social behavior of inbred mouse strains.

Li Ma, Sami Piirainen, Natalia Kulesskaya, Heikki Rauvala, Li Tian

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Transcriptional predictors of rescue behaviour in ants.The Journal of experimental biology · 2026
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  6. Review
  7. Phenotypic characteristics of commonly used inbred mouse strains.Journal of molecular medicine (Berlin, Germany) · 2020
    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.

Li MaNeuroscience Center, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland. li.ma@helsinki.fi.
Sami PiirainenNeuroscience Center, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland. sami.piirainen@helsinki.fi.
Natalia KulesskayaNeuroscience Center, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland. natalia.kulesskaya@helsinki.fi.
Heikki RauvalaNeuroscience Center, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland. heikki.rauvala@helsinki.fi.
Li TianNeuroscience Center, University of Helsinki, Viikinkaari 4, FIN-00014, Helsinki, Finland. li.tian@helsinki.fi.
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSocial deficit is one of the core symptoms of neuropsychiatric diseases, in which immune genes play an important role. Although a few immune genes have been shown to regulate social and emotional behaviors, how immune gene network(s) may jointly regulate sociability has not been investigated so far.

methodsTo decipher the potential immune-mediated mechanisms underlying social behavior, we first studied the brain microarray data of eight inbred mouse strains with known variations in social behavior and retrieved the differentially expressed immune genes. We then made a protein-protein interaction analysis of them to find the major networks and explored the potential association of these genes with the behavior and brain morphology in the mouse phenome database. To validate the expression and function of the candidate immune genes, we selected the C57BL/6 J and DBA/2 J strains among the eight inbred strains, compared their social behaviors in resident-intruder and 3-chambered social tests and the mRNA levels of these genes, and analyzed the correlations of these genes with the social behaviors.

resultsA group of immune genes were differentially expressed in the brains of these mouse strains. The representative C57BL/6 J and DBA/2 J strains displayed significant differences in social behaviors, DBA/2 J mice being less active in social dominance and social interaction than C57BL/6 J mice. The mRNA levels of H2-d1 in the prefrontal cortex, hippocampus, and hypothalamus and C1qb in the hippocampus of the DBA/2 J strain were significantly down-regulated as compared to those in the C57BL/6 J strain. In contrast, Polr3b in the hippocampus and Tnfsf13b in the prefrontal cortex of the DBA/2 J strain were up-regulated. Furthermore, C1qb, Cx3cl1, H2-d1, H2-k1, Polr3b, and Tnfsf13b were predicted to be associated with various behavioral and brain morphological features across the eight inbred strains. Importantly, the C1qb mRNA level was confirmed to be significantly correlated with the sociability in DBA/2 J but not in C57BL/6 J mice.

conclusionsOur study provided evidence on the association of immune gene network(s) with the brain development and behavior in animals and revealed neurobiological functions of novel brain immune genes that may contribute to social deficiency in animal models of neuropsychiatric disorders.

Indexed as

Social BehaviorAnimalsB-Cell Activating FactorBrainCX3C Chemokine Receptor 1CytokinesGene Expression ProfilingGene Expression RegulationH-2 AntigensMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMice, Inbred DBAMicroarray AnalysisOnline SystemsB-Cell Activating Factorcomplement 1q receptorCX3C Chemokine Receptor 1Cx3cr1 protein, mouseCytokinesH-2 AntigensMembrane GlycoproteinsReceptors, ChemokineReceptors, ComplementRNA, MessengerRNA Polymerase IIITnfsf13b protein, mouse

Identifiers

PMID25895500
PMCPMC4404243
OpenAlexW2032898989

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.