Immunogenetic Role of IL17A Polymorphism in the Pathogenesis of Recurrent Miscarriage

Interleukin-17A (IL17A) is a proinflammatory cytokine and is assumed to play an important role in fetal rejection. In order to evaluate the potential role of IL17A polymorphism in the pathogenesis of recurrent miscarriage (RM), serum IL17A levels were estimated by ELISA. Single-nucleotide polymorphi...

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Published in:Journal of clinical medicine Vol. 11; no. 24; p. 7448
Main Authors: Ali, Shafat, Majid, Sabhiya, Ali, Md Niamat, Banday, Mujeeb Zafar, Taing, Shahnaz, Wani, Saima, Almuqbil, Mansour, Alshehri, Sultan, Shamim, Kashif, Rehman, Muneeb U
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 15-12-2022
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Summary:Interleukin-17A (IL17A) is a proinflammatory cytokine and is assumed to play an important role in fetal rejection. In order to evaluate the potential role of IL17A polymorphism in the pathogenesis of recurrent miscarriage (RM), serum IL17A levels were estimated by ELISA. Single-nucleotide polymorphism was assessed by polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) using gene-specific primers and the EcoNI restriction enzyme. Serum IL17A levels were nonsignificantly (p > 0.5) low in RM patients compared with the control group. IL17A gene amplification by PCR yielded the undigested product of 815 bp, and its digestion with EcoNI enzyme produced 815, 529, 286, and 270 bp fragments for the GG genotype; 529, 286, and 270 bp fragments for the GA genotype; and 529 and 286 bp fragments for the AA genotype. The genotype frequency between the RM and control groups exhibited a significant difference (p = 0.001), whereas no significant difference was observed between allele frequencies in the two groups (p = 0.0954). These data suggest that the IL17A gene polymorphism exhibits no significant effect on IL17A gene expression. However, it significantly decreases and increases RM risk in the homozygous and recessive models, suggesting its potential pregnancy-protecting and -harming roles in the AA and GA + GG genotypes, respectively.
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ISSN:2077-0383
2077-0383
DOI:10.3390/jcm11247448