Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.
A, K., FA, M., MAN, K., MT, N., SM, N., N, B., STA, S., MJ, K., & S, H. (2026). Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.. Immunogenetics. https://doi.org/10.1007/s00251-026-01410-5
A K, FA M, MAN K, MT N, SM N, N B, et al. Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.. Immunogenetics. 2026; doi: 10.1007/s00251-026-01410-5
A K, FA M, MAN K, et al. Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.[J]. Immunogenetics. 2026. DOI: 10.1007/s00251-026-01410-5.
@article{a2026,
author = {Kainat A and Mian FA and Khan MAN and Nasim MT and Nurulain SM and Bibi N and Shah STA and Khan MJ and Hussain S},
title = {Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.},
journal = {Immunogenetics},
year = {2026},
doi = {10.1007/s00251-026-01410-5},
note = {PMID: 42402508},
}
TY - JOUR AU - Kainat A AU - Mian FA AU - Khan MAN AU - Nasim MT AU - Nurulain SM AU - Bibi N AU - Shah STA AU - Khan MJ AU - Hussain S TI - Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension. T2 - Immunogenetics PY - 2026 DO - 10.1007/s00251-026-01410-5 AN - PMID:42402508 ER -
Cytokines are crucial in regulating hypertension and vascular inflammation. The clinical significance of circulating IL-36γ levels and IL36G gene variants in relation to essential hypertension risk was assessed because IL-36γ has been associated with several cardiovascular diseases, while its role in essential hypertension is still unknown. Serum IL-36γ levels were determined by enzyme-linked immunosorbent assay, while IL36G polymorphisms were assessed by PCR-RFLP method in 264 patients with essential hypertension and 264 normotensive controls. Patients showed significantly elevated serum IL-36γ levels (p < 0.0001) when compared with the controls. Significant association between IL36G rs11690399 and rs11683399 polymorphisms and essential hypertension susceptibility were found through genotyping analysis, with combination genotypes (GT + TT) and (TG + GG) conferring an elevated risk of a disease. A 2.6-fold and a 1.9-fold increased risk of essential hypertension was observed to the T allele of rs11690399 and the G allele of rs11683399, respectively. Significantly higher levels of IL-36γ were associated with variant genotypes, suggesting a genotype-phenotype correlation. T-T and T-G were found to be a risk haplotype for essential hypertension by haplotype analysis. A causal relationship between increased IL-36γ and the risk of hypertension was shown by Mendelian randomization (OR = 1.0066; 95% CI: 1.0028-1.0104, p < 0.0001). A diagnostic performance for IL-36γ (AUC = 0.862) was found by ROC analysis, indicating its potential as a clinical biomarker. In conclusion, there is a significant association between essential hypertension and higher IL-36γ levels and IL36G polymorphisms. These results suggest that elevated circulatory IL-36γ may play a role in the pathophysiology of essential hypertension.