Evidence map›Paper›PMID 32174913›Full record

ArticleFrontiers in immunology2020

A Novel Microglia-Specific Transcriptional Signature Correlates With Behavioral Deficits in Neuropsychiatric Lupus.

Hadijat M Makinde, Deborah R Winter, Daniele Procissi, Elise V Mike, Ariel D Stock, Mary J Kando, Gaurav T Gadhvi, Steven Droho, Christina L Bloomfield, Salina T Dominguez and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  5. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
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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

14 authors at 3 institutions in 2 countries.

Hadijat M MakindeDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Deborah R WinterDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Daniele ProcissiDepartment of Radiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Elise V MikeDivision of Rheumatology, Department of Medicine, Albert Einstein College of Medicine, The Bronx, NY, United States.
Ariel D StockDivision of Rheumatology, Department of Medicine, Albert Einstein College of Medicine, The Bronx, NY, United States.
Mary J KandoDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Gaurav T GadhviDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Steven DrohoDepartment of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Christina L BloomfieldDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Salina T DominguezDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Maximilian G MayrDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Jeremy A LavineDepartment of Ophthalmology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Chaim PuttermanDivision of Rheumatology, Department of Medicine, Albert Einstein College of Medicine, The Bronx, NY, United States.
Carla M CudaDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Northwestern University · USAlbert Einstein College of Medicine · USWestern Galilee Hospital · IL

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
POSTDOCTORAL RHEUMATOLOGY TRAININGT32AR007611 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R · 2001 to 2022
$4.4M
The role of TWEAK and Fn14 in the Pathogenesis and Treatment of NeuropsychiatricR01AR065594 · NIAMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI PUTTERMAN, CHAIM · 2014 to 2018
$2.4M
The role of beta2-adrenergic receptor and interleukin-6 signaling in macrophage-driven choroidal neovascularizationK08EY030923 · NEI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LAVINE, JEREMY A · 2020 to 2024
$972k
FACSAria SORP Cell SorterS10OD011996 · OD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GOOLSBY, CHARLES L. · 2012 to 2012
$482k
The role of fas signaling in rheumatoid arthritisF32AR060169 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CUDA, CARLA M · 2010 to 2012
$118k
NCI NIH HHS P30 CA060553NEI NIH HHS K08 EY030923NIAMS NIH HHS F32 AR060169NIAMS NIH HHS R01 AR065594NIAMS NIH HHS T32 AR007611NIGMS NIH HHS T32 GM007288NIH HHS S10 OD011996
6 · The paper itself

Abstract

Neuropsychiatric symptoms of systemic lupus erythematosus (NP-SLE) affect over one-half of SLE patients, yet underlying mechanisms remain largely unknown. We demonstrate that SLE-prone mice (CReCOM) develop NP-SLE, including behavioral deficits prior to systemic autoimmunity, reduced brain volumes, decreased vascular integrity, and brain-infiltrating leukocytes. NP-SLE microglia exhibit numerical expansion, increased synaptic uptake, and a more metabolically active phenotype. Microglia from multiple SLE-prone models express a "NP-SLE signature" unrelated to type I interferon. Rather, the signature is associated with lipid metabolism, scavenger receptor activity and downregulation of inflammatory and chemotaxis processes, suggesting a more regulatory, anti-inflammatory profile. NP-SLE microglia also express genes associated with disease-associated microglia (DAM), a subset of microglia thought to be instrumental in neurodegenerative diseases. Further, expression of "NP-SLE" and "DAM" signatures correlate with the severity of behavioral deficits in young SLE-prone mice prior to overt systemic disease. Our data are the first to demonstrate the predictive value of our newly identified microglia-specific "NP-SLE" and "DAM" signatures as a surrogate for NP-SLE clinical outcomes and suggests that microglia-intrinsic defects precede contributions from systemic SLE for neuropsychiatric manifestations.

Indexed as

TranscriptomeAnimalsAssociation LearningBlood-Brain BarrierDisease Models, AnimalFemaleGenetic Predisposition to DiseaseGray MatterLupus Erythematosus, SystemicLupus Vasculitis, Central Nervous SystemMacrophagesMaze LearningMemory DisordersMiceMice, Inbred MRL lprMice, Mutant StrainsbehaviorDAMinterferonlupusmicrogliaNP-SLESLE

Identifiers

PMID32174913
PMCPMC7055359
OpenAlexW3008105794

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.