Ask about this productRelated genes to: IL31 antibody
- 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 antibody
Related articles to: IL31 antibody
- 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 - Ovarian cancer is the most lethal gynecological malignancy worldwide, largely due to late diagnosis and lack of effective population-level screening tools. Inflammatory cytokines regulate proliferation, apoptosis, angiogenesis, and immune surveillance, making inherited variation in cytokine pathways biologically plausible determinants of ovarian cancer susceptibility and progression. Since the early 2000s, numerous candidate-gene studies have evaluated polymorphisms of genes such as the interleukin () families, tumor necrosis factor alpha (), transforming growth factor beta 1 (), and components of the nuclear factor kappa B () signaling pathway and adhesion pathways, across diverse populations. In this review, we summarize these potential markers to give readers an overview showing accumulated evidence supports a coherent model in which genetically modulated inflammation is an integral driver of epithelial ovarian carcinogenesis. Collectively, studies reveal recurrent patterns of risk-increasing and risk-protective variants. Risky genotypes predicted to enhance pro-inflammatory, pro-angiogenic, or immunosuppressive signaling include rs16944 CC, rs1800795, rs2227306 TT, rs1126647 TT, rs11556218 GT/GG, rs4778889 CT/CC, rs10889677 AC/CC, rs4758680 CA/AA, rs28372698 TT, rs1800629 GA/AA, and peroxisome proliferator-activated receptor gamma () rs1801282 CG genotypes. Conversely, protective variants tend to dampen inflammatory tone or rebalance cytokine networks, including rs17561 GT/TT, rs4848300 CT/CC, rs3783553 insertion/insertion, rs7596684 CT/CC, rs1880242 GT/TT, rs7977932 CG/GG, rs1800469 CT/TT, selectin E () rs5361 AC, intercellular adhesion molecule 1 () rs5498 AG genotypes and specific haplotypes. Beyond risk , several polymorphisms appear predictive of clinical features, including tumor stage, cytoreductive resectability and recurrence, highlighting potential prognostic relevance. Notably, associations are often population-specific, reflecting differences in allelic frequencies and linkage disequilibrium across ethnic groups, underscoring the need for cross-ethnic replication. Further investigations may ultimately enable further improved the prevention, early detection, and personalized management of ovarian cancer. - Source: PubMed
Chang Wen-ShinTsai Chia-WenChen Jaw-ChyunWang Yun-ChiBau DA-Tian - - Source: PubMed
Publication date: 2026/04/28
Ebi NanaKogame ToshiakiIshida-Yamamoto AkemiAkasaka EijiroKabashima Kenji - Observational studies suggest an association between Coronavirus Disease 2019 (COVID-19) and polymyositis (PM), but causal inference s limited by confounding. This study adopted a multilevel exploratory framework to investigate potential relationships. We used two-sample Mendelian randomization (MR) to assess the causal effect of severe COVID-19 on PM, multi-omic analyses to screen for potential mediators, and retrospectively compared hematological profiles between severe and non-sever COVID-19 cases. - Source: PubMed
Publication date: 2026/04/09
Chen MiaomiaoLi HongmeiTong XiaZhang Xin