Evidence of association of macrophage migration inhibitory factor gene polymorphisms with systemic lupus erythematosus

Sánchez, Elena; Gómez, Luis Alberto Ramírez; Nevot, López; Gonzalez-Gay,; Sabio, JM; Ortego-Centeno, Norbérto; Enrique, Rafael; Anaya, Juan Manuel; González-Escribano, M F; Koeleman, Bobby P. C.; Martin, Jose-Ezequiel

doi:10.1038/sj.gene.6364310

Cited by 89 publications

(80 citation statements)

References 26 publications

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“…Elevated circulating levels of MIF have been observed in rheumatoid arthritis, atherosclerosis, asthma, lupus, diabetes, colitis, sepsis, cancer, and cardiovascular and infectious diseases (15)(16)(17)(18)(19)(20). Genetic evidence further supports the involvement of MIF in disease.…”

Section: Macrophage Migration Inhibitory Factor (Mif)mentioning

confidence: 77%

“…Functional polymorphisms in the MIF gene affect disease severity, such that individuals inheriting a high expressor allele have increased levels of MIF in circulation and often show severe disease manifestation. Therapeutic relief achieved through blocking MIF activity by genetic, immunological, and pharmacological means further supports the involvement of MIF in disease pathology (17,(21)(22)(23)(24).…”

Section: Macrophage Migration Inhibitory Factor (Mif)mentioning

confidence: 99%

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A Novel Allosteric Inhibitor of Macrophage Migration Inhibitory Factor (MIF)

Bai

Asojo

Cirillo³

et al. 2012

Journal of Biological Chemistry

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Background: MIF is a pro-inflammatory cytokine implicated in autoimmune diseases. Results: A small molecule that binds to MIF and inhibits its cytokine activities was identified. Conclusion:The inhibitor binds in a unique region on MIF and reveals a new way to block the cytokine activities of MIF. Significance: The inhibitor is a valuable tool to design MIF-directed therapeutics for inflammatory diseases.

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Section: Macrophage Migration Inhibitory Factor (Mif)mentioning

confidence: 77%

Section: Macrophage Migration Inhibitory Factor (Mif)mentioning

confidence: 99%

A Novel Allosteric Inhibitor of Macrophage Migration Inhibitory Factor (MIF)

Bai

Asojo

Cirillo³

et al. 2012

Journal of Biological Chemistry

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“…Written informed consent was obtained from all subjects, and the study was approved by the local ethics committee of each center. Demographic characteristics of the patients and controls in each population have been described previously (5,18,19).…”

Section: Methodsmentioning

confidence: 99%

Association of a CD24 gene polymorphism with susceptibility to systemic lupus erythematosus

Sánchez¹,

Abelson²,

Sabio³

et al. 2007

Arthritis & Rheumatism

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Objective. To determine the potential role of the CD24 A57V gene polymorphism in systemic lupus erythematosus (SLE).Methods. We studied 3 cohorts of Caucasian patients and controls. The Spanish cohort included 696 SLE patients and 539 controls, the German cohort included 257 SLE patients and 317 controls, and the Swedish cohort included 310 SLE patients and 247 controls. The CD24 A57V polymorphism was genotyped by polymerase chain reaction, using a predeveloped TaqMan allele discrimination assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.Results. In the Spanish cohort there was a statistically significant difference in the distribution of the CD24 V allele between SLE patients and controls (OR 3.6 [95% CI 2.13-6.16], P < 0.0001). In addition, frequency of the CD24 V/V genotype was increased in SLE patients compared with controls (OR 3.7 [95% CI 2.16-6.34], P < 0.00001). We sought to replicate this association with SLE in a German population and a Swedish population. A similar trend was found in the German group. The CD24 V/V genotype and the CD24 V allele were more frequent in SLE patients than in controls, although this difference was not statistically significant. No differences were observed in the Swedish group. A meta-analysis of the Spanish and German cohorts demonstrated that the CD24 V allele has a risk effect in SLE patients (pooled OR 1.25 [95% CI 1.08-1.46], P ‫؍‬ 0.003). In addition, homozygosity for the CD24 V risk allele significantly increased the effect (pooled OR 2.19 [95% CI 1.50-3.22], P ‫؍‬ 0.00007).Conclusion. These findings suggest that the CD24 A57V polymorphism plays a role in susceptibility to SLE in a Spanish population.Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease with a complex pathogenesis involving multiple genetic and environmental factors. The disease is characterized by enhanced autoantibody production, abnormalities of immune/inflammatory system function, and inflammation in several organs. Al-

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“…An SNP (−173G>C; rs755622) and a CATT tetranucleotide repeat (−794CATT [5][6][7][8] ) in the promoter region have been tested for their associations with inflammatory diseases. Associations for one or both polymorphisms with systemic-onset juvenile idiopathic arthritis, rheumatoid arthritis, atopy, psoriasis, systemic lupus erythematosus and obesity have been reported [15][16][17][18][19][20][21] and suggest that these SNPs may have some functional relevance.…”

Section: Introductionmentioning

confidence: 99%

Effect of macrophage migration inhibitory factor (MIF) gene variants and MIF serum concentrations on the risk of type 2 diabetes: results from the MONICA/KORA Augsburg Case–Cohort Study, 1984–2002

et al. 2007

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Aims/hypothesis Macrophage migration inhibitory factor (MIF) is a central mediator of innate immunity. Our aim was to investigate the triangular association between MIF genotypes, circulating MIF concentrations and incident type 2 diabetes, and to use a Mendelian randomisation approach to assess the causal role of MIF. Methods Using a case-cohort design within the population-based MONICA/KORA Augsburg Study, based on 502 individuals with incident type 2 diabetes (293 men, 209 women) and 1,632 non-cases (859 men, 773 women), we determined MIF serum levels at baseline and genotyped four MIF single nucleotide polymorphisms (SNPs). Results The C allele of SNP rs1007888 (3.8 kb 3′ of the translation termination codon) was associated with increased circulating MIF. MIF genotype rs1007888CC was associated with an increased risk of type 2 diabetes in women [hazard ratio (95% CI) 1.74 (1.02-2.97)], but not in men [1.17 (0.75-1.81)]. Elevated MIF serum levels were associated with higher type 2 diabetes risk also only in women [HR (95% CI) 1.95 (1.15-3.29) comparing extreme quartiles after multiple adjustment], but not in men (p for interaction 0.039). The association between MIF levels and incident type 2 diabetes was significantly higher in obese women (111 cases, 147 non-cases) compared with nonobese women (98 cases, 626 non-cases; p for BMI interaction 0.0002). Conclusions/interpretation The consistent triangular relationship between genotypes, serum levels and incident type 2 diabetes in women indicates that MIF may play a causal role in the aetiology of type 2 diabetes and that elevated MIF levels confer a higher disease risk.

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Evidence of association of macrophage migration inhibitory factor gene polymorphisms with systemic lupus erythematosus

Cited by 89 publications

References 26 publications

A Novel Allosteric Inhibitor of Macrophage Migration Inhibitory Factor (MIF)

A Novel Allosteric Inhibitor of Macrophage Migration Inhibitory Factor (MIF)

Association of a CD24 gene polymorphism with susceptibility to systemic lupus erythematosus

Effect of macrophage migration inhibitory factor (MIF) gene variants and MIF serum concentrations on the risk of type 2 diabetes: results from the MONICA/KORA Augsburg Case–Cohort Study, 1984–2002

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