IL Variant May Serve as Genetic Biomarker for Severity, Joint Involvement in Psoriasis


Findings are based on a case-control study carried out in Brazil.

The interleukin (IL)36G rs7584409 variant may be used as a potential genetic biomarker to predict severity and joint involvement in patients with psoriasis, new study results suggest.

Findings were published in Molecular Immunology and based on data collected from 154 patients with psoriasis and 154 controls in Brazil.

“[Psoriasis] shows traces of autoimmune and autoinflammatory disease, with both innate and adaptive immune response overlapping and even potentiating each other,” authors explained. Although the etiology of psoriasis is not completely understood, genetic, epigenetic, and environmental factors all likely play a role.

In addition, “the activation of interferon gamma (IFN-γ), interleukin (IL)-36, and IL-23/IL-17 axis are pivotal events in the pathophysiology of [psoriasis],” they added.

IL-36 has gained further importance in the condition’s pathophysiology as it plays a role in the interaction between the innate and adaptive immune response. Genetic variants linked with psoriasis are involved in different biological processes, the authors noted, including those in genes encoding cytokines and its susceptibility.

To better understand the frequency of the rs13392494 intron C>T and rs7584409 3’UTR A>G variants of the IL36G gene and their link with the susceptibility and severity of psoriasis and the presence of psoriatic arthritis in Brazilian patients, researchers carried out a case-control study. The investigators used the Psoriasis Area and Severity Index (PASI) to assess severity of the condition.

Analyses revealed:

  • Patients were older (P < .001) and had higher body mass index (P < .001) than controls
  • 95.8% of the patients had plaque psoriasis, 16.1% had psoriatic arthritis, and 27.9% had PASI > 10
  • The IL36G rs1339294 variant showed no association with psoriasis in all genetic models while the IL36G rs7584409 variant showed a protective effect in psoriasis
  • The G allele of the IL36G rs7584409 in the dominant model was positively associated with PASI > 10 (P = .031)
  • Patients with the GG genotype of the IL36G rs7584409 variant had an approximate 5.0 times greater chance of psoriatic arthritis than those with the AA genotype (P = .014)
  • The C/A haplotype in a recessive model (CACA vs C/G and T/A carriers) was associated with psoriasis (P = .035) while the C/G haplotype in a dominant model (C/A carriers vs C/G and T/A carriers) showed a protective effect for psoriasis (P = .041)

Overall, “the G allele of the IL36G rs7584409 variant was associated with protection to psoriasis; however, in patients with psoriasis, this same allele was associated with moderate to severe disease and psoriatic arthritis,” the authors wrote.

They also note that additional factors involved in the etiology of psoriasis that could be present among patients may exert a role in the regulation of IL36G gene expression.

The finding that those without the disease carrying the AG + GG genotypes showed about 48% of protection to psoriasis while those with the disease carrying the G allele (AG+GG genotypes) had moderate to severe disease and psoriatic arthritis is in line with knowledge that the IL-1 superfamily of cytokines and receptors can be pro-inflammatory or protective, the researchers explained.

The study sample was derived from a single health unit from the South Brazilian population, meaning results may not be generalizable.

“More investigation in genetically different populations is required to clarify the exact molecular origins of psoriasis and how it develops into psoriatic arthritis,” the authors wrote.

Overall, the current data “suggested that the IL36G rs7584409 variant may be used as a possible genetic biomarker to predict severity and joint involvement of psoriasis,” they concluded.


Moreira CR, de Alcântara CC, Flauzino T, et al. IL36G genetic variant is independently associated with susceptibility, severity and joint involvement in psoriasis. Mol Immunol. Published online June 6, 2023. doi:10.1016/j.molimm.2023.05.010

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