Macrophage Migration Inhibitory Factor

Alternative Names

  • MIF
  • MMIF
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OMIM Number

153620

Gene Map Locus
22q11.23

Description

The Macrophage Migration Inhibitory Factor (MIF) gene encodes a lymphokine involved in numerous cellular process such as cell-mediated immunity, immunoregulation, and inflammation.  It regulates the function of macrophages in host defense through the suppression of anti-inflammatory effects of glucocorticoids.  This lymphokine forms a complex with the JAB1 protein, which may play a role in integrin signaling pathways.  Recent studies have also pointed out to a role of this gene in processes beyond immune regulation, including cell proliferation and differentiation, and tumorigenesis. 

Studies have supported the notion that MIF-directed therapies might offer new treatment opportunities for human diseases in the future.

Molecular Genetics

MIF gene is located on the long arm of chromosome 22.  It is a small gene consisting of three exons separated by introns of only 189 and 95 bp, and it covers less than 1 kb.  The encoded protein called macrophage migration inhibitory factor is made up of 115 amino acids with a molecular mass of 12476 Da.  The MIF protein contains two catalytic motifs.  The 27-amino-acid motif, located at the N-terminus, functions as a phenylpyruvate tautomerase that can catalyze the conversion of 2-carboxy-2,3-dihydroindole-5,6-quinone (dopachrome) into 5,6-dihydroxyindole-2-carboxylic acid (DHICA).  The second is a Cys-Ala-Leu-Cys catalytic site between residues 57 and 60 that appears to function as a disulfide reductase. 

Two polymorphic sites within the promoter region regulate gene expression.  These are a CATT repeat sequence at -794, and the SNP -173G/C.  The presence of more than 5 repeats of the CATT sequence and the -173C allele have been known to associate with increased susceptibility to various inflammatory and autoimmune diseases, as well as prostrate and gastric cancers.  

Epidemiology in the Arab World

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Other Reports

Saudi Arabia

Abdallah et al., (2016) enrolled 124 Saudi patients with rheumatic heart disease (RHD) in a pilot study at pediatric cardiology clinics in Al Madina between 2013 and 2014.  The control consisted of 202 healthy Saudi participants.  All samples were genotyped for MIF-173 (rs755622) and MIF-794 (rs5844572) polymorphisms.  The authors found that the age of onset was significantly greater for MIF -173C allele carriers than non-MIF-173C allele carriers in the group of RHD patients.  The mean ages of onset of carriers of C-allele and non-carriers were 9.2 ± 1.6 and 7.5 ± 2.4, respectively.  No significant association between the tetranucleotide variation and disease age of onset was found.  The authors surmised that variations in MIF influenced disease severity and progression and recommended further studies to address and analyze the disease stage and patient age.

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