Ask about this productRelated genes to: IL17E antibody
- Gene:
- IL25 NIH gene
- Name:
- interleukin 25
- Previous symbol:
- IL17E
- Synonyms:
- IL-25, IL-17E
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2014-11-19
Related products to: IL17E antibody
Related articles to: IL17E antibody
- Eosinophilic chronic rhinosinusitis (ECRS) is characterized by refractory nasal polyps and severely impaired mucociliary clearance (MCC). The molecular mechanisms underlying the modulation of mucociliogenesis following IL-4/13 blockade with dupilumab remain poorly understood, notwithstanding its proven clinical efficacy. - Source: PubMed
Publication date: 2026/05/15
Fujita RikutoIshino TakashiOda TakashiKawasumi TomohiroNishida ManabuHoribe YuichiroChikuie NobuyukiTaruya TakayukiHamamoto TakaoUeda TsutomuTakeno Sachio - Asthma is a heterogeneous chronic inflammatory airway disease affecting over 300 million people worldwide. The airway epithelium serves as the primary interface with environmental stimuli and responds by releasing epithelial-derived alarmins, thymic stromal lymphopoietin (TSLP), interleukin-33 (IL-33), and interleukin-25 (IL-25), which act as upstream regulators of both innate and adaptive immune responses. Current therapies targeting downstream inflammatory mediators demonstrate limited efficacy in severe and refractory asthma, necessitating novel approaches targeting upstream pathways. - Source: PubMed
Publication date: 2026/05/26
H R SnehaDhanush YaravaRajaram CuddapahNelson Kumar SadhuSiva Ganesh Vakkalagadda - Tuft cells are rare chemosensory epithelial cells distributed throughout mucosal barriers. Recent findings have established their roles in detecting helminths, protists, and bacteria and in regulating innate immunity and tissue physiology via secretion of effector molecules like IL-25, eicosanoids, and acetylcholine. This Review explores critical outstanding topics in gastrointestinal tuft cell biology, including what their evolved functions are beyond helminth sensing, how they detect different pathogens and dietary challenges, and why small intestinal tuft cells proliferate dramatically during type 2 responses. In addition, we explore how their differentiation is regulated by diverse epithelial-intrinsic and epithelial-extrinsic signals, whether they communicate with neurons in the intestine, and what roles they play in adaptive immunity. By organizing recent findings around these key topics, we highlight both progress and gaps in the understanding of how tuft cells integrate lumenal signals to regulate barrier immunophysiology. - Source: PubMed
Publication date: 2026/05/22
Thompson Thornton Wvon Moltke Jakob - Crosstalk between hepatocellular carcinoma (HCC) and the tumor microenvironment (TME) is pivotal for the initiation and management of HCC. The infiltration and function of natural killer (NK) cells in the TME are frequently hindered. However, it is unclear whether a crucial regulatory factor originating from HCC cells directly modulates NK cell activity to evade immune surveillance. In this study, we found that mannose-binding lectin 2 (MBL2) expression was markedly decreased in HCC and positively correlated with HCC prognosis. MBL2 inhibited the proliferation and migration of HCC cells intracellularly. Human and murine co-culture systems of HCC and NK cells were established to demonstrate that secreted MBL2 recruited and activated NK cells in the TME, particularly upregulating the infiltration of NKp46+ NK cells. Furthermore, secreted MBL2 promoted the production of IL-13 and IL-25 by NK cells, resulting in a decrease in exhausted cytotoxic T lymphocytes. Mechanistically, MBL2 interacts with the integrin β1 receptor, activating the FAK/AKT pathway and increasing PD-L1 expression on NK cells. Our discovery identifies MBL2 as an NK cell-activating cytokine, initiating the integrin β1/FAK/AKT pathway in NK cells and reshaping an immune-activated microenvironment of HCC. Strategies to up-regulate MBL2 may enhance the anti-PD-L1 immunotherapy efficacy and serve as a potential therapeutic approach for HCC. - Source: PubMed
Publication date: 2026/05/20
Liao HangyuYang JunCai LeiChi LuhaoWang ChunmingXu YuyanXie JunchengChen KunlingPei JingyuanJiang ZeshengPan MingxinZhao Liang - Group 2 innate lymphoid cells (ILC2s) support tissue homeostasis and type 2 inflammation. ILC2s, which are found in many tissues, adapt to local cues to perform tissue-specific functions. Intestinal ILC2s rapidly respond to helminth and protozoan infections via cross-talk with tuft cells, but the mechanism guiding this adaptation remains unclear. Here, we identify Notch signaling, triggered by the ligand Delta-like 1 on goblet cells, as a key regulator of gut ILC2 specialization in mice. Loss of the Notch signaling protein RBPJ did not impair ILC2 development but altered the expression of interleukin-33 (IL-33) and IL-25 receptors (ST2 and IL-17RB, respectively) on gut ILC2s. This increased sensitivity to IL-33, promoted IL-5 and IL-13 production, and drove the expansion of gut eosinophils and goblet cells. Moreover, RBPJ-deficient ILC2s failed to respond to tuft cell-derived IL-25 after colonization. Thus, RBPJ-dependent Notch responsiveness in ILC2s regulates intestinal tissue adaptation and primes the tuft cell-ILC2 circuit for intestinal homeostasis. - Source: PubMed
Publication date: 2026/05/15
Burrows KyleNgai LouisTai Siu LingChiaranunt PailinChen Edward L YKamath ManjulaZúñiga-Pflücker Juan CarlosMortha Arthur