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Macrophage migration inhibitory factor in Nodding syndrome
Gil Benedek1, Mahmoud Abed El Latif1, Keren Miller1
1Tissue Typing and Immunogenetics Unit, Department of Genetics, Hadassah Medical Organization and Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel.
Plos Neglected Tropical Diseases
|October 18, 2021
Summary
Nodding syndrome (NS), an autoimmune epilepsy, involves Onchocerca Volvulus. While a high-expression Macrophage Migration Inhibitory Factor (MIF) genotype may protect against NS, elevated MIF plasma levels correlate with disease severity and neuroinflammation.
Area of Science:
- Neuroimmunology
- Genetics
- Infectious Diseases
Background:
- Nodding syndrome (NS) is a severe childhood epilepsy linked to Onchocerca Volvulus (Ov) infection and neuroinflammation.
- Emerging evidence suggests NS may be an autoimmune epilepsy, with autoantibodies targeting glutamate receptors and Leiomodin-I.
- Genetic factors, including HLA associations, play a role in NS susceptibility and protection.
Purpose of the Study:
- To investigate the role of Macrophage Migration Inhibitory Factor (MIF) gene polymorphisms and plasma levels in Nodding Syndrome (NS).
- To explore the potential dual role of MIF in the pathogenesis of NS, considering both genetic predisposition and immune response.
Main Methods:
- Genotyping of two functional MIF gene polymorphisms (-794 CATT repeat and -173 G/C SNP) in 49 NS patients and 51 controls from South Sudan.
- Measurement of plasma MIF levels in NS patients and healthy controls.
- Analysis of the interplay between MIF and HLA associations in NS.
Main Results:
- The high-expression MIF -173C genotype was less frequent in NS patients than in controls, suggesting a protective genetic association.
- Plasma MIF levels were significantly elevated in NS patients compared to healthy controls.
- HLA associations with NS were found to be dominant over MIF associations.
Conclusions:
- MIF may have a dual role in NS: a protective genetic component via high-expression genotypes and a detrimental role in autoimmunity and neuroinflammation through elevated plasma levels.
- These findings contribute to understanding the complex pathogenesis of NS, involving genetic susceptibility, parasitic infection, and immune dysregulation.
- Further research is warranted to elucidate the precise mechanisms of MIF's involvement in NS and its potential as a therapeutic target.
