Ask about this productRelated genes to: IL1F5 antibody
- Gene:
- IL36RN NIH gene
- Name:
- interleukin 36 receptor antagonist
- Previous symbol:
- IL1F5
- Synonyms:
- FIL1, FIL1(DELTA), FIL1D, IL1HY1, IL1RP3, IL1L1, IL-1F5, IL36RA, MGC29840
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-02
- Date modifiied:
- 2019-04-23
Related products to: IL1F5 antibody
Related articles to: IL1F5 antibody
- Pustular psoriasis (IL-36/Th17) and atopic dermatitis (Th2) are associated with different but partially overlapping inflammatory pathways. Sequential expression of these phenotypes in the same patient is uncommon. We describe a 64-year-old woman with longstanding psoriasis vulgaris, asthma, allergic rhinitis, and a family history of atopy who developed generalized pustular psoriasis after biologic treatments. Genetic testing identified a novel, previously unreported heterozygous IL36RN frameshift variant, c.319del (p.Leu107Serfs65). Over subsequent months, the pustular phenotype was replaced by chronic, intensely pruritic, xerotic, eczematous dermatitis fulfilling the Hanifin-Rajka criteria. Serial biopsies demonstrated mild spongiosis and an eosinophil-rich superficial perivascular infiltrate. Risankizumab and adalimumab were temporally associated with pustular exacerbations, whereas dupilumab was followed by worsening of the eczematous phenotype without recurrent pustulation. Methotrexate 15 mg weekly, which restrains both axes, together with topical treatment was associated with sustained near-complete clearance through Month 12. To our knowledge, this is the first report of a three-class biologic paradox in a single patient. Sequential single-pathway blockade in a genetically destabilized immune network may disinhibit alternative effector arms with cytokine shunting. Inborn errors of immunity should be considered in refractory inflammatory dermatoses-even in geriatric patients-and pathway-specific biologics used cautiously when the underlying immune architecture is monogenically perturbed. - Source: PubMed
Publication date: 2026/08/31
Çalıcıoğlu FurkanÇalıcıoğlu NeşecanDoğan Muhammet EnsarTekin YücelErtaş Ragıp - Classic deficiency of interleukin-36 (IL-36) receptor antagonist (DITRA) is characterized by severe, recurrent generalized pustular psoriasis (GPP) with systemic inflammation and is typically caused by biallelic variants. However, monoallelic c.115+6T>C and c.28C>T variants of have also been reported to underlie DITRA. To the best of our knowledge, no cases of a heterozygous c.28C>T variant presenting with the unilateral localization of symptoms have been reported. Our present case emphasize that -related disease should be considered even with the atypical skin symptoms, thereby broadening the spectrum of DITRA. - Source: PubMed
Omi MichiyaTakeichi TakuyaTanahashi KanaAdachi HidesadaKambara TakeshiMuro YoshinaoAkiyama Masashi - To explore genotype-phenotype associations of variants and clinical outcomes of spesolimab treatment in acrodermatitis continua of Hallopeau (ACH). - Source: PubMed
Publication date: 2026/07/13
Deng XuanChen YushaLiu XinliXiong JianxiaHu RunluLiao SijianLi WeiHuang Kun - - Source: PubMed
Demirsoy Evren OdyakmazSerinbaş Semanur ÇakırBayramgürler DilekBayrak Busra YaprakKıran Rebiay - The interleukin (IL) 23/T helper (Th) 17 axis is the cornerstone of psoriasis pathogenesis, but molecular heterogeneity across different ethnicities remains poorly defined. - Source: PubMed
Publication date: 2026/07/02
Chen Chung-HanLee Meng-SuiChang Wen-YuCho Yung-TsuLu Yea-TingHuang Wen-LiChu Chia-YuTsai Tsen-FangKrueger James GChan Tom C