Evidence map›Paper›PMID 27570219›Full record

ArticleClinical immunology (Orlando, Fla.)2017

CSF-1R inhibition attenuates renal and neuropsychiatric disease in murine lupus.

Samantha A Chalmers, Jing Wen, Justine Shum, Jessica Doerner, Leal Herlitz, Chaim Putterman

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The MRL Model: A Valuable Tool in Studies of Autoimmunity-Brain Interactions.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  5. Article
  6. Current cell therapies for systemic lupus erythematosus.Stem cells translational medicine · 2024
    Review
  7. Review
  8. Article
  9. Roles of macrophages in lupus nephritis.Frontiers in pharmacology · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

6 authors at 3 institutions in 1 country.

Samantha A ChalmersAlbert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, NY, USA.
Jing WenAlbert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, NY, USA.
Justine ShumMontefiore Medical Center, Department of Medicine, Bronx, NY, USA.
Jessica DoernerAlbert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, NY, USA.
Leal HerlitzCleveland Clinic, Department of Pathology, Cleveland, OH, USA.
Chaim PuttermanAlbert Einstein College of Medicine, Department of Microbiology and Immunology, Bronx, NY, USA; Albert Einstein College of Medicine, Division of Rheumatology, Bronx, NY, USA. Electronic address: chaim.putterman@einstein.yu.edu.
Albert Einstein College of Medicine · USCleveland Clinic · USMontefiore Medical Center · US

Funding

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
NIAMS NIH HHS R01 AR065594
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease that can affect multiple end organs. Kidney and brain are two of the organs most commonly involved in SLE. Past studies have suggested the importance of macrophages in the pathogenesis of lupus nephritis (LN). Furthermore, as the immune effectors of the brain, microglia have been implicated in pathways leading to neuropsychiatric SLE (NPSLE). We depleted macrophages and microglia using GW2580, a small colony stimulating factor-1 receptor (CSF-1R) kinase inhibitor, in MRL-lpr/lpr (MRL/lpr) mice, a classic murine lupus model that displays features of both LN and NPSLE. Treatment was initiated before the onset of disease, and mice were followed for the development of LN and neurobehavioral dysfunction throughout the study. Treatment with GW2580 significantly ameliorated kidney disease, as evidenced by decreased proteinuria, BUN, and improved renal histopathology, despite equivalent levels of IgG and C3 deposition in the kidneys of treated and control mice. We were able to confirm macrophage depletion within the kidney via IBA-1 staining. Furthermore, we observed specific improvement in the depression-like behavioral deficit of MRL/lpr mice with GW2580 treatment. Circulating antibody and autoantibody levels were, however, not affected. These results provide additional support for the role of macrophages as a potentially valuable therapeutic target in SLE. Inhibiting CSF-1 receptor signaling would be more targeted than current immunosuppressive therapies, and may hold promise for the treatment of renal and neuropsychiatric end organ disease manifestations.

Indexed as

AnimalsAnisolesAntibodies, AntinuclearBrainChromatinComplement System ProteinsCytokinesDepressionDisease Models, AnimalFemaleImmunoglobulin GKidneyLocomotionLupus NephritisLupus Vasculitis, Central Nervous SystemMacrophages5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamineAnisolesAntibodies, AntinuclearChromatinComplement System ProteinsCytokinesImmunoglobulin GPyrimidinesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorCSF-1RLupus nephritisMacrophagesNeuropsychiatric lupusSLE

Identifiers

PMID27570219
PMCPMC5326697
OpenAlexW2508464043

What OpenQuestion holds

Textmetadata
LicenceTDM
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.