Evidence map›Paper›PMID 26466956›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Cholesterol-Independent Suppression of Lymphocyte Activation, Autoimmunity, and Glomerulonephritis by Apolipoprotein A-I in Normocholesterolemic Lupus-Prone Mice.

Leland L Black, Roshni Srivastava, Trenton R Schoeb, Ray D Moore, Stephen Barnes, Janusz H Kabarowski

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. High-density lipoprotein infusion protects from acute graft-versus-host disease in experimental allogeneic hematopoietic cell transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  9. Article
  10. The Effect of Lipid Metabolism on CD4Mediators of inflammation · 2021
    Review
  11. Lipid Metabolism Profiles in Rheumatic Diseases.Frontiers in pharmacology · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Autoimmunity in 2015.Clinical reviews in allergy & immunology · 2016
    Review
  20. Review
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 2 institutions in 1 country.

Leland L BlackDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294;
Roshni SrivastavaDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294;
Trenton R SchoebDepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294; and.
Ray D MooreDepartment of Pharmacology and Toxicology, Targeted Metabolomics and Proteomics Laboratory, University of Alabama at Birmingham, Birmingham, AL 35294.
Stephen BarnesDepartment of Pharmacology and Toxicology, Targeted Metabolomics and Proteomics Laboratory, University of Alabama at Birmingham, Birmingham, AL 35294.
Janusz H KabarowskiDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294; janusz@uab.edu.
University of Alabama at Birmingham · USTarget (United States) · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Training Program in Cardiovascular PathophysiologyT32HL007918 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BALLINGER, SCOTT W. · 1999 to 2018
$3.6M
The role of the G2A receptor in AtherosclerosisR01HL088642 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KABAROWSKI, JANUSZ H · 2007 to 2011
$1.8M
SPECT: POLYPHENOLS: SOY &MENARCHE,0STEOPOR, GREEN TEA&BREAST CANCER, NEURODIS S10RR019231 · NCRR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNES, STEPHEN · 2004 to 2004
$465k
Replacement of GC Mass SpectrometerS10RR027940 · NCRR · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI THOMAS, MICHAEL J · 2010 to 2010
$209k
NCI NIH HHS 5P30CA12197NCI NIH HHS P30 CA012197NCRR NIH HHS 1S10RR027940NCRR NIH HHS S10 RR019231NCRR NIH HHS S10 RR027940NCRR NIH HHS S10RR19231NHLBI NIH HHS R01 HL088642NHLBI NIH HHS T32 HL007918NIAMS NIH HHS P30 AR048311NIDDK NIH HHS P30 DK 079337NIDDK NIH HHS P30 DK079337
6 · The paper itself

Abstract

Apolipoprotein (Apo)A-I, the major lipid-binding protein of high-density lipoprotein, can prevent autoimmunity and suppress inflammation in hypercholesterolemic mice by attenuating lymphocyte cholesterol accumulation and removing tissue-oxidized lipids. However, whether ApoA-I mediates immune-suppressive or anti-inflammatory effects under normocholesterolemic conditions and the mechanisms involved remain unresolved. We transferred bone marrow from systemic lupus erythematosus (SLE)-prone Sle123 mice into normal, ApoA-I-knockout (ApoA-I(-/-)) and ApoA-I-transgenic (ApoA-I(tg)) mice. Increased ApoA-I in ApoA-I(tg) mice suppressed CD4(+) T and B cell activation without changing lymphocyte cholesterol levels or reducing major ApoA-I-binding oxidized fatty acids. Unexpectedly, oxidized fatty acid peroxisome proliferator-activated receptor γ ligands 13- and 9-hydroxyoctadecadienoic acid were increased in lymphocytes of autoimmune ApoA-I(tg) mice. ApoA-I reduced Th1 cells independently of changes in CD4(+)Foxp3(+) regulatory T cells or CD11c(+) dendritic cell activation and migration. Follicular helper T cells, germinal center B cells, and autoantibodies were also lower in ApoA-I(tg) mice. Transgenic ApoA-I also improved SLE-mediated glomerulonephritis. However, ApoA-I deficiency did not have the opposite effects on autoimmunity or glomerulonephritis, possibly as the result of compensatory increases in ApoE on high-density lipoprotein. We conclude that, although compensatory mechanisms prevent the proinflammatory effects of ApoA-I deficiency in normocholesterolemic mice, increasing ApoA-I can attenuate lymphocyte activation and autoimmunity in SLE independently of cholesterol transport, possibly through oxidized fatty acid peroxisome proliferator-activated receptor γ ligands, and it can reduce renal inflammation in glomerulonephritis.

Indexed as

AnimalsApolipoprotein A-IApolipoproteins EAutoantibodiesAutoimmunityB-LymphocytesBone Marrow TransplantationCell MovementCholesterolDendritic CellsGas Chromatography-Mass SpectrometryLinoleic AcidsLipoproteins, HDLLupus NephritisLymphocyte ActivationMice13-hydroxy-9,11-octadecadienoic acidApolipoprotein A-IApolipoproteins EAutoantibodiesCholesterolLinoleic AcidsLipoproteins, HDLPPAR gamma

Identifiers

PMID26466956
PMCPMC4637240
OpenAlexW2409072674

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.