Evidence map›Paper›PMID 22127710›Full record

ArticleArthritis and rheumatism2011

Dual effect of the macrophage migration inhibitory factor gene on the development and severity of human systemic lupus erythematosus.

Antoine Sreih, Rana Ezzeddine, Lin Leng, Avery LaChance, Geraldine Yu, Yuka Mizue, Lakshman Subrahmanyan, Bernardo A Pons-Estel, Anna-Karin Abelson, Iva Gunnarsson and 10 more

Abstract readComparative StudyMulticenter Study
In one paragraph

Article in Arthritis and rheumatism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Pathogenic role of MIF receptor (CD74) expressing T cells in inflammatory arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. MIF contribution to progressive brain diseases.Journal of neuroinflammation · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Macrophage migration inhibitory factor in Nodding syndrome.PLoS neglected tropical diseases · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

5 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

20 authors at 9 institutions in 3 countries.

Antoine SreihYale University School of Medicine, New Haven, Connecticut 06520, USA.
Rana Ezzeddine
Lin Leng
Avery LaChance
Geraldine Yu
Yuka Mizue
Lakshman Subrahmanyan
Bernardo A Pons-Estel
Anna-Karin Abelson
Iva Gunnarsson
Elisabet Svenungsson
Joshua Cavett
Stuart Glenn
Lin Zhang
Ruth Montgomery
Andras Perl
Jane Salmon
Marta E Alarcón-Riquelme
John B Harley
Richard Bucala
Yale University · USOklahoma Medical Research Foundation · USKarolinska Institutet · SEBristol-Myers Squibb (United States) · USCentro Científico Tecnólogico - Rosario · ARCincinnati Children's Hospital Medical Center · USHospital for Special Surgery · USSUNY Upstate Medical University · USUppsala University · SE

Funding

HLA GENE COMPLEMENTATION IN PRIMARY SJOGREN'S AND LUPUSR01AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KOTTYAN, LEAH CLAIRE, WEIRAUCH, MATTHEW TYSON · 1987 to 2025
$7.8M
SNP Confirmation and High Throughput Genotyping CoreP30AR053483 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GUTHRIDGE, JOEL MARVIN · 2007 to 2017
$6.7M
Mechanisms of Rheumatoid Synovial Fibroblast ActivationR01AR049610 · NIAMS · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2002 to 2018
$5.0M
Genetic Linkage in LupusR37AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2005 to 2014
$4.2M
INNATE AND ADAPTIVE MECHANISMS IN ARTHRITISR01AR050498 · NIAMS · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2004 to 2013
$3.6M
IMMUNE FUNCTION AND BIODEFENSE IN CHILDREN. ELDERLY AND IMMUNOCOMPROMI-266050031N01AI050031 · NIAID · EMORY UNIVERSITY · PI LARSEN, CHRISTOPHER · 2006 to 2006
–
NIAID NIH HHS N01 AI050031NIAID NIH HHS N01-AI-50031NIAID NIH HHS R01 AI024717NIAID NIH HHS R37 AI024717NIAMS NIH HHS AR-049610NIAMS NIH HHS AR-050498NIAMS NIH HHS P30 AR053483NIAMS NIH HHS R01 AR049610NIAMS NIH HHS R01 AR050498
6 · The paper itself

Abstract

objectiveTo study the effect of the innate cytokine macrophage migration inhibitory factor (MIF) on the susceptibility and severity of systemic lupus erythematosus (SLE) in a multinational population of 1,369 Caucasian and African American patients.

methodsTwo functional polymorphisms in the MIF gene, a -794 CATT(5-8) microsatellite repeat (rs5844572) and a -173 G/C single-nucleotide polymorphism (rs755622), were assessed for association with SLE in 3,195 patients and healthy controls. We also measured MIF plasma levels in relation to genotypes and clinical phenotypes, and assessed Toll-like receptor 7 (TLR-7)-stimulated MIF production in vitro.

resultsBoth Caucasians and African Americans with the high-expression MIF haplotype -794 CATT(7)/-173*C had a lower incidence of SLE (in Caucasians, odds ratio [OR] 0.63, 95% confidence interval [95% CI] 0.53-0.89, P = 0.001; in African Americans, OR 0.46, 95% CI 0.23-0.95, P = 0.012). In contrast, among patients with established SLE, reduced frequencies of low-expression MIF genotypes (-794 CATT(5)) were observed in those with nephritis, those with serositis, and those with central nervous system (CNS) involvement when compared to patients without end-organ involvement (P = 0.023, P = 0.005, and P = 0.04, respectively). Plasma MIF levels and TLR-7-stimulated MIF production in vitro reflected the underlying MIF genotype of the studied groups.

conclusionThese findings suggest that MIF, which has both proinflammatory properties and macrophage and B cell survival functions, exerts a dual influence on the immunopathogenesis of SLE. High-expression MIF genotypes are associated with a reduced susceptibility to SLE and may contribute to an enhanced clearance of infectious pathogens. Once SLE develops, however, low-expression MIF genotypes may protect from ensuing inflammatory end-organ damage.

Indexed as

Severity of Illness IndexAdultBlack or African AmericanCase-Control StudiesCross-Sectional StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansLupus Erythematosus, SystemicMacrophage Migration-Inhibitory FactorsMaleMiddle AgedPhenotypePolymorphism, Single NucleotideTumor Necrosis Factor-alphaMacrophage Migration-Inhibitory FactorsTumor Necrosis Factor-alpha

Identifiers

PMID22127710
PMCPMC3228269
OpenAlexW2023917813

What OpenQuestion holds

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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.