IL-9 Recombinant Protein
- Known as:
- Interleukin-9 Recombinant Protein
- Catalog number:
- ZR-40-536
- Product Quantity:
- 0.002 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IL-9 Recombinant Protein
Ask about this productRelated genes to: IL-9 Recombinant Protein
- 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 Recombinant Protein
Related articles to: IL-9 Recombinant Protein
- 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 - Tularemia is a rare zoonotic infection with marked geographic clustering and long interepidemic periods. Pediatric data, particularly those on host immune responses during active disease and treatment, remain scarce. The authors aimed to evaluate clinical characteristics and treatment-associated cytokine dynamics in children with tularemia. In the present multicenter prospective study conducted in Türkiye, 40 pediatric patients with laboratory-confirmed tularemia and nine age- and sex-matched healthy controls were enrolled between April 2023 and November 2024. Clinical features, exposure history, and treatment outcomes were recorded. Serum cytokine levels, including interleukin (IL)-6, IL-2, IL-9, IL-5, IL-13, tumor necrosis factor-α, IL-10, interferon (IFN)-γ, IL-4, and IL-22, were measured using a multiplex bead-based assay and compared between patients and controls, between good and poor outcome groups, and longitudinally before and after therapy. A good outcome was defined as complete clinical resolution without suppuration, the need for surgical intervention, or relapse, whereas a poor outcome was defined as clinical nonresolution or progression. A total of 24 (60%) participants had a good outcome, and 16 (40%) had a poor outcome. Although baseline cytokine levels did not differ between groups, paired analyses revealed significant posttreatment reductions in IFN-γ (P = 0.018), IL-6 (P = 0.018), and IL-10 (P = 0.032), consistent with resolution of infection-associated immune activation. A poor outcome was associated with increased exposure to natural water sources and a higher frequency of suppurative lymphadenopathy requiring surgical drainage. Baseline cytokine profiles did not predict treatment response; however, dynamic changes in IFN-γ, IL-6, and IL-10 were associated with clinical recovery. These findings highlight the importance of longitudinal immune monitoring and provide insight into immune dynamics in pediatric tularemia. - Source: PubMed
Publication date: 2026/06/11
Cakici OzlemAykac KubraSeyrek Bera EnesYılmaz İsmail CemDemir Osman OguzEvcili İremCanavar Yıldırım TuğçeYıldırım MuzafferErdeniz Emine HafizeYasar Durmus SevgiSahin AslıhanOcal Demir SevliyaCengiz Ali BulentGürsel MaydaGürsel İhsanOzsurekci Yasemin - Pectic rhamnogalacturonan-I (RG-I) is a dietary fiber that modulates the gut-immune axis. This study evaluates a novel variant of RG-I from chicory root (chRG-I). In a randomized, double-blind, placebo-controlled trial, 55 healthy adults were stratified by habitual fiber intake and baseline levels before receiving 500 mg/day of chRG-I or placebo for four weeks. Primary endpoints included fecal counts. Secondary outcomes assessed fecal metabolites, systemic immune cell activation markers, and gastrointestinal symptoms. To provide mechanistic insights, donor-matched fecal samples were used in fermentation and Caco-2/peripheral blood mononuclear cell co-culture gut barrier models. Supplementation with chRG-I induced a statistically significant bifidogenic effect, with absolute levels peaking at week three, and lower levels of some fecal short-chain fatty acids (SCFA) compared to placebo. However, donor-matched fermentations with chRG-I confirmed robust production of SCFA and reduction of branched-chain fatty acids levels (BCFA). Systemically, chRG-I upregulated HLA-DR expression on myeloid dendritic cells. Clinically, chRG-I was well-tolerated and slightly improved stool consistency compared to placebo. In an intestinal barrier challenge model, chRG-I fermentates (a pool of metabolites including SCFA and fragments of chRG-I) protected barrier integrity, modulated the cytokine milieu away from a predominantly pro-inflammatory response, as characterized by increased IL4 and IL22 and reduced IL9, IL17A, and IL21. Supplementation with a low dose of chRG-I is well-tolerated, beneficially modulates the gut microbiome - which can protect the intestinal barrier, and subtly enhances systemic immune readiness, suggesting that chRG-I may have benefits as a functional food ingredient. - Source: PubMed
Publication date: 2026/05/13
Kerezoudi Evangelia NMcKay SueKurt SetaDe Kreek MaaikeDe Medts JelleVerstrepen LynnGhyselinck JonasMeulebroek Lieven VanCalame WimAlbers RuudMercenier AnnickBrummer Robert JRangel Ignacio - This review provides an overview of recent advances in understanding T-cell inflammation in atopic dermatitis (AD), a common chronic inflammatory skin disease. After recognizing their cognate antigen in the acute phase of the disease, the homing of T cells from the circulation into the skin via cutaneous lymphocyte antigen (CLA) is the prerequisite to skin inflammation and subsequent systemic and local, tissue resident, memory (TRM) formation. Initial observations suggest that antigen presentation occurs in structures such as induced skin-associated lymphoid tissue (iSALT), in addition to lymphatic organs. Aside from environmental antigens, such as aeroallergens, other antigen sources also appear to play a role: humoral and cellular responses to microbial antigens and autoantigens are discussed to drive and shape skin inflammation in AD. In-depth characterization of differentiated, activated Th2 cells in AD shows their ability to recognize different signals from epithelial cells directly. The heterogeneity of patients with antigen sensitizations and T-cell phenotypes is believed to influence therapeutic success. This suggests that a more precise characterization of patient subgroups would enable targeted, individualized therapy. - Source: PubMed
Publication date: 2026/06/03
Baumann Phila CaraRoesner Lennart Matthias - Pathogenesis of cerebral malaria, the most severe form of Plasmodium infection, has been well studied in experimental rodent models by using P. falciparum homologue P. berghei ANKA(PbA). Although Th-9 (CD4+ IL-9+) cells have been reported to be expanded during PbA infection, their functional effect on other immune cells, specifically macrophages, dendritic cells, and Myeloid Derived Suppressor Cells (MDSCs), and the crucial factors behind Th-9 differentiation are yet to be deciphered, which ultimately determines the disease burden. Here, we investigate how IL-9 regulates the immune-metabolic state of MDSCs and how MDSCs, through a positive feedback loop, control Th-9 differentiation during experimental cerebral malaria (ECM) in rodents upon infection with PbA. IL-9 played an important role in MDSC expansion and particularly PMN-MDSC proliferation. It also enhanced pro-inflammatory phenotype within MDSCs. Apart from MDSCs, IL9 also induced the inflammatory phenotypes in macrophages and dendritic cells, thus exacerbating inflammation, leading to higher host morbidity. Neutralizing IL9 in vivo reduced immunopathology and increased host survival during PbA infection. Conversely, depleting MDSCs led to a decrease of Th-9 cell population, their transcription factors, and down-regulated their migratory potentials, thus suggesting that these two cells work in a positive feedback mechanism. Elevated secretion of IL-1β from MDSCs was defined as a pivotal factor in controlling Th-9 differentiation. The findings highlight the potent role of IL-9 as a key component in host immune response modulation during ECM and hint toward a possible new adjunct therapeutic formulation by blocking IL-9. - Source: PubMed
Publication date: 2026/06/09
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