Ask about this productRelated genes to: IL31 protein
- Gene:
- IL31 NIH gene
- Name:
- interleukin 31
- Previous symbol:
- -
- Synonyms:
- IL-31
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-06
- Date modifiied:
- 2014-11-19
Related products to: IL31 protein
Related articles to: IL31 protein
- Dermatomyositis (DM) is an inflammatory myopathy frequently accompanied by pruritus, which can be severe, treatment-refractory, and associated with significant impairment in quality of life. Interleukin-31 (IL-31) has emerged as a key mediator of itch and has been implicated in the inflammatory pathways of dermatomyositis, suggesting a potential therapeutic role for IL-31 receptor blockade. - Source: PubMed
Publication date: 2026/05/11
Nigro AlexandraDayanan JasperSilva IsabelSaini AariaKhattri Saakshi - Interleukin (IL)-31 has emerged as a pivotal mediator of pruritus. Since its initial identification, substantial progress has been made in elucidating the role of IL-31 in itch pathophysiology, particularly its direct effects on peripheral sensory neurons. Elevated IL-31 expression has been documented in a wide range of pruritic skin diseases, including atopic dermatitis, prurigo nodularis, and systemic disorders. Beyond its pruritogenic activity, IL-31 is increasingly recognized as a neuroimmune cytokine that links immune-cell activation to sensory-neuronal circuits and, in some contexts, may also exert immunomodulatory effects. IL-31 signals through a heterodimeric receptor complex composed of IL-31 receptor α and oncostatin M receptor β, activating downstream pathways. In sensory neurons, IL-31 receptor signaling defines a distinct pruritic pathway, but emerging human transcriptomic data indicate that IL-31-responsive neurons are more heterogeneous than the canonical murine NP3 subset, highlighting an important translational consideration. In this review, we summarize current knowledge regarding IL-31 biology, including its cellular sources, receptor expression, and signaling mechanisms, and discuss its role in both pruritic and non-pruritic diseases. We further evaluate therapeutic strategies targeting the IL-31/IL-31 receptor axis and consider the emerging concept that IL-31 blockade may relieve itch while simultaneously disinhibiting dendritic cell-driven type 2 inflammatory programs in selected contexts. - Source: PubMed
Publication date: 2026/05/05
Irie HiroyukiKabashima Kenji - Canine atopic dermatitis is a common chronic inflammatory skin disease characterized by pruritus and recurrent erythema, yet objective blood biomarkers for monitoring disease activity remain limited. In this study, we evaluated serum cytokine profiles and their associations with clinical severity in client-owned dogs with atopic dermatitis. A total of 143 dogs were enrolled, including 28 healthy and 115 dogs with atopic dermatitis. The atopic dermatitis group was further categorized into untreated dogs ( = 27; no systemic therapy for ≥4 weeks) and systemically treated dogs ( = 88). Serum concentrations of IFN-γ, IL-10, IL-13, IL-31, and TGF-β1 were measured using an enzyme-linked immunosorbent assay. Group differences were assessed using the Kruskal-Wallis test with Bonferroni-adjusted post hoc comparisons, and correlations with the pruritus visual analog scale (pVAS) and the Canine Atopic Dermatitis Extent and Severity Index-04 (CADESI-04) were analyzed using Spearman's rank correlation. Serum IFN-γ, IL-13, and IL-31 concentrations differed significantly among groups ( < 0.001, = 0.001, and = 0.004, respectively). IFN-γ and IL-13 concentrations were lower in treated dogs than in healthy dogs and untreated dogs, whereas IL-31 concentrations were higher in dogs with atopic dermatitis than in healthy dogs, regardless of treatment status. In correlation analyses, the pVAS showed a negative correlation with IFN-γ (r = -0.239, = 0.004) and a positive correlation with IL-31 (r = 0.173, = 0.039), while CADESI-04 showed a negative correlation with IFN-γ (r = -0.252, = 0.002). IL-10 and TGF-β1 did not show significant differences among groups or correlations with clinical indices. These findings suggest that serum IL-31 may reflect pruritus-related immune signaling that can persist despite clinical improvement. While IFN-γ may show a weak negative correlation with clinical severity indices, its potential association with chronic dermatologic changes, such as lichenification, requires further investigation in relation to disease chronicity. Together, these results indicate that circulating cytokine profiles and clinical indices do not necessarily change in parallel and that selected cytokines may provide complementary information when interpreting disease activity in canine atopic dermatitis. These profiles should be interpreted while considering the diverse immunomodulatory mechanisms of the systemic therapy administered. - Source: PubMed
Publication date: 2026/04/13
Ko Jae-YunKang Min-HeePark Hee-Myung - Atopic dermatitis (AD) is a chronic inflammatory dermatitis underpinned by Type 2 inflammation driven by cytokines such as IL-4 and IL-13. It is characterized by skin barrier dysfunction, Th2 immune deviation, and pruritus. While biologics and oral Janus kinase (JAK) inhibitors demonstrate high therapeutic efficacy by targeting cytokines that exert their effects via the JAK, specifically IL-4, IL-13, and IL-31, comprehensive disease control requires additional approaches that modulate JAK-independent pathways. Factors such as TNF-α, IL-25, IL-33, microbial antigens, and physical stimuli activate mitogen-activated protein kinase and nuclear factor-κB signaling in a JAK-independent manner, sustaining the disease activity. Consequently, in some cases, a strategy incorporating topical treatment that inhibits JAK-independent pathways is indispensable alongside systemic treatment. One potential strategy of this kind involves the aryl hydrocarbon receptor (AhR), ligand-activated transcription factor. Under Th2-polarized conditions, the expression of indoleamine 2,3-dioxygenase 1 (IDO1) is downregulated, limiting the availability of tryptophan-derived metabolites. This scarcity of endogenous AhR ligands subsequently compromises physiological AhR signaling. Tapinarof, a therapeutic AhR-modulating agent (TAMA), activates AhR without generating excessive reactive oxygen species. This exerts multiple effects: enhancing antioxidant defenses via nuclear factor erythroid 2-related factor 2 (NRF2) activation, restoring barrier dysfunction, suppressing Th2 inflammation, and correcting abnormalities associated with pruritus-related molecules. Furthermore, clinical trials of tapinarof have demonstrated improvement of the disease activity and pruritus, with efficacy intensifying over long-term treatment. Although adverse events such as folliculitis, acne, contact dermatitis, and headache occur, they are generally manageable by adjusting the frequency of application based on their reversibility and time of onset. Moreover, considering potential antagonism by IL-24 induced by tapinarof, combining tapinarof with systemic agents, topical therapies, or phototherapy may serve to optimize the therapeutic effects. In conclusion, AhR functions as a molecular hub integrating AD pathology, and the TAMA tapinarof expands therapeutic strategies in the treatment of AD. - Source: PubMed
Publication date: 2026/04/29
Tsuji GakuFuyuno YokoKawamura KojiYumine AyakoTakemura MasakiMitamura YasutakaYamamura KazuhikoNakahara Takeshi - We previously identified transmembrane protein 45b (Tmem45b) as a pain-related molecule essential for mechanical pain hypersensitivity but not for thermal pain hypersensitivity. A subset of Tmem45b is expressed in TRPV1-positive primary afferents, which are specialized in transmitting thermal pain and specific types of itch. Here, we examined the involvement of Tmem45b in itch perception. - Source: PubMed
Publication date: 2026/04/28
Maruyama TomoyukiYoshida AkariSunami ShogoUra AkihiroKurosaki HiromichiKawamata Tomoyuki