Macrophage migration inhibitory factor polymorphism (rs755622) in alopecia areata: a possible role in disease prevention

• Published in: Archives of Dermatological Research Vol. 311; no. 8; pp. 589 - 594
• Main Authors: Rajabi, Fateme, Amoli, Mahsa M., Robati, Reza M., Almasi-nasrabadi, Mina, Jabalameli, Navid
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.10.2019; Springer Nature B.V
• Subjects: Adolescent; Adult; Aged; Alleles; Alopecia; Alopecia Areata - genetics; Alopecia Areata - immunology; Alopecia Areata - prevention & control; Autoimmune diseases; Autoimmunity - genetics; Baldness; Case-Control Studies; Cytokines; Dermatology; Female; Follicles; Gene polymorphism; Genetic Predisposition to Disease; Genotype; Hair; Hair Follicle - immunology; Hair Follicle - pathology; Hair loss; Healthy Volunteers; Humans; Immune privilege; Immune Privilege - genetics; Inflammation; Intramolecular Oxidoreductases - genetics; Intramolecular Oxidoreductases - immunology; Leukocyte migration; Macrophage migration inhibitory factor; Macrophage Migration-Inhibitory Factors - genetics; Macrophage Migration-Inhibitory Factors - immunology; Male; Medicine; Medicine & Public Health; Middle Aged; Natural killer cells; Original Paper; Polymorphism, Single Nucleotide; Preservation; Scalp; Transcription; Young Adult; Autoimmunity; Genetic association study; Hair follicle; Immune privilege; Natural killer cells
• ISSN: 0340-3696; 1432-069X; 1432-069X
• DOI: 10.1007/s00403-019-01934-9

Alopecia areata (AA) is an organ-specific autoimmune disease that targets the bulb of the hair follicles and results in non-scarring hair loss that can range from patchy lesions to involvement of the entire scalp. AA develops when the hair follicles lose their physiologic state of immune privilege. One of the key factors that help in maintaining this immune privilege by suppressing natural killer cells is macrophage migration inhibitory factor (MIF). Surprisingly, MIF is also known to provoke autoimmunity by upregulating cytokines. To address this dilemma and understand the exact nature of the involvement of MIF in disease pathogenesis we investigated the association of MIF gene polymorphisms (− 173 G > C, rs755622) with AA by conducting a case–control study of 274 subjects. We observed that the frequency of the C allele in the patients was significantly lower than the control group (0.15, 0.23, respectively, p  = 0.01) and the combined frequencies of the CC and GC genotypes (dominant Mendelian pattern) had the most prevalent difference between the two groups (odds ratio 0.60, 95% confidence interval 0.36–0.99; p  = 0.048).Since the C allele is associated with higher MIF transcription levels, this could infer that MIF is more likely to attribute to the preservation of the immune privilege rather than acting as a proinflammatory factor.