Navigating IL-6: From molecular mechanisms to therapeutic breakthroughs

Swaroop, Akey Krishna; Negi, Preeya; Kar, Ayushi; Mariappan, Esakkimuthukumar; Natarajan, Jawahar; Namboori P.K., Krishnan; Selvaraj, Jubie

doi:10.1016/j.cytogfr.2023.12.007

Cited by 7 publications

(1 citation statement)

References 143 publications

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“…Polymorphisms in the promoter of the IL6 gene that determine individual differences in transcription regulation and gene expression, and thereby the intensity of cytokine production, shape the predisposition to certain diseases [32]. According to the literature, the four main single nucleotide polymorphisms of the IL6 gene promoter that collectively influence the transcription of this gene are −2954G > C, −1363G > T, −597G > A (rs1800797), and −572G > C (rs1800796) [32][33][34][35]. The IL6 rs1800795 (−174G > C) polymorphism is located in what is known as the negative regulatory domain (region −225 to −164) near the cAMP response element (CRE).…”

Section: Discussionmentioning

confidence: 99%

No Association of Polymorphisms in the Genes Encoding Interleukin-6 and Interleukin-6 Receptor Subunit Alpha with the Risk of Keloids in Polish Patients

Dmytrzak,

Lewandowska,

Boroń

et al. 2024

IJMS

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A keloid is a benign fibroproliferative hypertrophy of scar tissue that extends outside the original wound and invades adjacent healthy skin. Keloid formation is thought to be a complex process including overactivity of the interleukin-6 signaling pathway and genetic susceptibility. The aim of the study was to investigate possible associations between rs1800797, rs1800796, and rs1800795 polymorphisms in the promoter of the IL6 gene encoding interleukin-6 and the rs2228145 polymorphism in the IL6R gene encoding the interleukin-6 receptor subunit alpha with the predisposition to keloids in Polish patients. The genetic polymorphisms were identified either using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) or sequencing of samples of genomic DNA extracted from blood leukocytes of 86 adult patients with keloids and 100 newborns comprising a control group. No significant differences in the distributions of IL6 or IL6R alleles or genotypes were found between keloid patients and newborn controls. There were also no significant differences between both groups in the distribution of IL6 haplotypes. The IL6 rs1800797, rs1800796 and rs1800795 and IL6R rs2228145 polymorphisms were not found to predispose individuals in the study group to keloids. IL6 promoter haplotypes were not found to be associated with a higher risk of keloids in the studied group.

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