IL-9, human recombinant
- Known as:
- Interleukin-9, H. sapiens Rec.
- Catalog number:
- BC-282
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- kamyia
- Gene target:
- IL-9 human recombinant
Related genes to: IL-9, human recombinant
- Gene:
- IL9 NIH gene
- Name:
- interleukin 9
- Previous symbol:
- -
- Synonyms:
- IL-9, HP40, P40
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-11
- Date modifiied:
- 2016-10-05
Related products to: IL-9, human recombinant
Related articles to: IL-9, human recombinant
- Breast cancer (BC) is the most common malignant neoplasm in women worldwide and in Peru. Beyond hormonal and genetic factors, cytokines play a key role in tumor aggressiveness and therapeutic resistance. However, evidence on circulating cytokine profiles in Latin American populations is limited. - Source: PubMed
Publication date: 2026/06/09
Vela-Ruiz Jose MMorante ZaidaFerreyra YomaliGalvez-Villanueva Marco AValencia FernandoCampos-Tineo J JhaninaCallapiña De Paz MarianaCórdova-Salazar Ariana AlessandraMarcos-Carbajal PoolMoreno Lujan Joan MPantoja Lazaro Andy REscobar Caipo Laura GFlores Trujillo Gustavo ACusma Quintana Teresa NDe La Cruz-Vargas Jhony AGomez Henry LSoto Alonso - Allergic diseases, including asthma and food allergies, pose a global public health challenge. However, the complex immunopathological mechanisms have not been fully elucidated yet. Although T helper 2 (Th2) cells are regarded as central drivers, they cannot fully explain the clinical heterogeneity and therapeutic resistance of these diseases. This review aimed to systematically illustrate the key roles and regulatory mechanisms of T helper 9 (Th9) cells and their effector cytokine interleukin-9 (IL-9) in various allergic diseases. Th9 cells differentiate under the synergistic induction of transforming growth factor-β (TGF-β) and interleukin-4 (IL-4), and their specific transcription factors (such as Spi-1 proto-oncogene (PU.1), Interferon Regulatory Factor 4 (IRF4)) and epigenetic modifications jointly regulate IL-9 expression. IL-9 acts on mast cells, B cells, eosinophils, and epithelial cells, forming a positive-feedback inflammatory amplification loop that connects adaptive immunity to structural tissue cells. Although drug development targeting IL-9 (such as enokizumab) has faced challenges, intervention strategies targeting key nodes of this axis remain a highly promising research direction. The Th9/IL-9 axis, as a critical hub linking immune activation and pathological tissue changes, provides a new theoretical framework for understanding the heterogeneity of allergic diseases and represents a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/23
Yu ChengshengXue ZimengHe RuiWu HuimeiTu Jiajie - Lung cancer is among the most common malignancies globally, exhibiting the greatest rates of incidence and death compared to all other cancers. Cigarette smoking is a significant causal factor in lung cancer; yet the molecular mechanisms via which smoking facilitates lung cancer development remain mainly ambiguous. In this study, we used different concentrations of cigarette smoke extract (CSE) to A549 cells. Compared with the control group, the total STAT3 expression remained basically unchanged. However, we found that phosphorylated STAT3 (p-STAT3), interleukin-9 (IL-9), and miR-155-5p all increased obviously, while the expression of suppressor of cytokine signaling 1 (SOCS1) decreased greatly. Moreover, the epithelial marker E-cadherin was downregulated, while the mesenchymal markers Vimentin and α-SMA were upregulated, indicating the induction of epithelial-mesenchymal transition (EMT). Interventions with STAT3 siRNA, a miR-155-5p inhibitor, or a SOCS1 overexpression plasmid reversed these changes. Similarly, co-treatment with an IL-9-neutralizing antibody attenuated CSE-induced alterations in p-STAT3, SOCS1, miR-155-5p, and EMT markers. In a nude mouse xenograft model, CSE exposure significantly enhanced tumor growth and EMT phenotypes, whereas IL-9 neutralization reduced tumorigenicity of CSE-treated A549 cells. Collectively, these findings demonstrate that cigarette smoke promotes lung cancer progression by inducing EMT through the IL-9-regulated STAT3/miR-155-5p/SOCS1 feedback loop, providing novel mechanistic insight and potential therapeutic targets for smoking-related lung cancer. - Source: PubMed
Publication date: 2026/06/19
Li ZhanLuo YajunLiu XinTan JiangWang HailanLu JiWei WencaiZhang QinshuZhang TingZhang QingbiBai Jun - Systemic lupus erythematosus (SLE) is a progressive antibody-mediated autoimmune disease characterized by systemic immune complex deposition. A subset of SLE patients has elevated CD4+IL-9+ T cells as well as increased levels of secreted interleukin (IL)-9 and IL9 messenger RNA compared with healthy control subjects. However, because IL-9 can have both pro- and anti-inflammatory effects in autoimmune disease, its function in SLE is unclear. We use the MRL/lpr murine model of SLE to demonstrate that IL-9 exhibits protective activity in the early stages of disease. Treatment of these mice with an IL-9 neutralizing antibody from 6 to 12 wk of age results in an expansion of immune cells, leading to exacerbation of disease. In contrast, treatment with anti-IL-9 from 6 to 18 wk of age does not significantly alter disease course compared with isotype control. Anti-IL-9 antibody treatment of these mice results in reduced systemic IL-2 levels, IL-9+ type 2 innate lymphoid cells, and regulatory T cells in the kidney, suggesting an IL-9-dependent suppressive cellular circuit similar to that observed in rheumatoid arthritis. Importantly, supplementation of IL-2 during IL-9 blockade recovers regulatory T cell numbers and limits disease. Together, these data demonstrate an IL-9-dependent suppressive circuit that is evident early in the development of SLE which may be amenable to manipulation to achieve a therapeutic benefit. - Source: PubMed
Krishnan Maya SZhou BaohuaYang DongmingGoncalves Joao IJackson Kaitlyn GXue Gloria RTurner Matthew JKaplan Mark H - Atopic dermatitis (AD) is often associated with ocular surface disease (OSD). Dupilumab, an IL-4Rα inhibitor, is an effective treatment for AD but it sometimes induces dupilumab-associated OSD (DAOSD). DAOSD may associate with a paucity of conjunctival goblet cells or altered immune response; however, the mechanism remains undetermined. Therefore, we aimed to identify ophthalmological alterations and to explore the potential mechanisms of DAOSD in AD patients receiving dupilumab. - Source: PubMed
Publication date: 2026/06/11
Cho Yung-TsuChan Tom CChen Wei-LiChu Hsiao-SangChu Chia-Yu