Evidence map›Paper›PMID 20805419›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

The detrimental effects of IFN-α on vasculogenesis in lupus are mediated by repression of IL-1 pathways: potential role in atherogenesis and renal vascular rarefaction.

Seth G Thacker, Celine C Berthier, Deborah Mattinzoli, Maria Pia Rastaldi, Matthias Kretzler, Mariana J Kaplan

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
5.5field-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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Interaction of miR-181b andBioMed research international · 2020
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  7. Article
  8. Review
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  10. Article
  11. Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Endothelial cells: potential novel regulators of renal inflammation.American journal of physiology. Renal physiology · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

13 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

6 authors at 3 institutions in 2 countries.

Seth G ThackerDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Celine C Berthier
Deborah Mattinzoli
Maria Pia Rastaldi
Matthias Kretzler
Mariana J Kaplan
University of Michigan–Ann Arbor · USFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITMichigan Medicine · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TODD, ROBERT F · 2001 to 2010
$5.9M
NETs in the development of lupus and its cardiovascular complicationsR01HL088419 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 2009 to 2016
$3.1M
Molecular Progression Predictors in the Chronic Renal Insufficiency CohortR01DK079912 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KRETZLER, MATTHIAS · 2008 to 2012
$2.8M
NCI NIH HHS P30 CA046592NCI NIH HHS P30 CA46592NHLBI NIH HHS HL088419NHLBI NIH HHS R01 HL088419NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30 AR48310NIDDK NIH HHS P30 DK081943NIDDK NIH HHS R01 DK079912
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is characterized by increased vascular risk due to premature atherosclerosis independent of traditional risk factors. We previously proposed that IFN-α plays a crucial role in premature vascular damage in SLE. IFN-α alters the balance between endothelial cell apoptosis and vascular repair mediated by endothelial progenitor cells (EPCs) and myeloid circulating angiogenic cells (CACs). In this study, we demonstrate that IFN-α promotes an antiangiogenic signature in SLE and control EPCs/CACs, characterized by transcriptional repression of IL-1α and β, IL-1R1, and vascular endothelial growth factor A, and upregulation of IL-1R antagonist and the decoy receptor IL-1R2. IL-1β promotes significant improvement in the functional capacity of lupus EPCs/CACs, therefore abrogating the deleterious effects of IFN-α. The beneficial effects from IL-1 are mediated, at least in part, by increases in EPC/CAC proliferation, by decreases in EPC/CAC apoptosis, and by preventing the skewing of CACs toward nonangiogenic pathways. IFN-α induces STAT2 and 6 phosphorylation in EPCs/CACs, and JAK inhibition abrogates the transcriptional antiangiogenic changes induced by IFN-α in these cells. Immunohistochemistry of renal biopsies from patients with lupus nephritis, but not anti-neutrophil cytoplasmic Ab-positive vasculitis, showed this pathway to be operational in vivo, with increased IL-1R antagonist, downregulation of vascular endothelial growth factor A, and glomerular and blood vessel decreased capillary density, compared with controls. Our study introduces a novel putative pathway by which type I IFNs may interfere with vascular repair in SLE through repression of IL-1-dependent pathways. This could promote atherosclerosis and loss of renal function in this disease.

Indexed as

Neovascularization, PhysiologicAdultAtherosclerosisCell DifferentiationEndothelial CellsFemaleGene ExpressionGene Expression ProfilingGene Expression RegulationHumansImmunohistochemistryInterferon-alphaInterleukin-1Interleukin 1 Receptor Antagonist ProteinKidneyLupus Erythematosus, SystemicInterferon-alphaInterleukin-1Interleukin 1 Receptor Antagonist ProteinReceptors, Interleukin-1Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID20805419
PMCPMC2978924
OpenAlexW2122995291

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.