Rat Interleukin 9,IL-9 ELISA KIT
- Known as:
- Rat Interleukin 9,Interleukin-9 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- csb-e07294r
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Cusabio Elisa
- Gene target:
- Rat Interleukin 9 IL-9 ELISA KIT
Related genes to: Rat Interleukin 9,IL-9 ELISA KIT
- 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: Rat Interleukin 9,IL-9 ELISA KIT
Related articles to: Rat Interleukin 9,IL-9 ELISA KIT
- Myasthenia gravis (MG) is a clinically and immunologically heterogeneous autoimmune disease and there is little known about the differential effects of cytokines in disease subgroups. This study aimed to compare serum cytokine profiles across distinct MG subgroups, including early-onset MG (EOMG), late-onset MG (LOMG), muscle-specific kinase antibody-positive MG (MuSK-MG), thymoma-associated MG (TAMG), and healthy controls (HC) in order to distinguish and determine relatively specific targets for the disease subgroups. - Source: PubMed
Publication date: 2026/07/01
Cebi MerveDurmus HacerÇakar ArmanGünver Mehmet GüvenParman YesimDeymeer FezaSaruhan-Direskeneli Güher - Multiple sclerosis (MS) is a chronic autoimmune disorder of CNS with demyelination, neurodegeneration and compartmentalized inflammatory disorder. Excessive T-helper cell (CD4) activation and unregulated cytokine signaling play a key role in its onset and progression. These changes impair communication between peripheral immune cells and CNS resident microglia, astrocytes and oligodendrocytes. This review provides an overview on the contribution of specific subsets of T-helper cells to MS pathology/immunity. Th1 cells release interferon-γ and lymphotoxin, that stimulate activation of myeloid cells/antigen presentation. Activated by IL-23, the Th17 cells produce IL-17A/F that lowers the blood-brain barrier (BBB) integrity, recruit neutrophils and monocytes, and enhance microglial killing. Activation of CD4 T cells leads to activation of B cells via T follicular helper cells which couple these processes through the production of IL-21 and CXCR5. This leads to the development of tissue-like aggregates and intrathecal antibody production. T-cell plasticity adds to epitope spreading as well as chronic inflammation, IL-22, IL-9, IL-1β, IL-6, and TGF-β (these are additional mediators involved in the regulation of effector phenotypes). In MS, the regulation of dendritic cell co-stimulation and of glial activation often does not work. This is due to the lack of control of dendritic-cells co-stimulation and the lack of regulation of glial activation by regulatory pathways such as FOXP3 regulatory T cells and Tr1 cells that secrete IL-10 and TGF-Beta. The review also explores the cytokine network biomarkers, CSF and serum signatures and single-cell immune states, as well as existing and new drugs. These include migration blockade, targeting of S1P-receptors, anti-CD20 therapy, targeting of Th17/GM-CSF and JAK-STAT pathways, low-dose IL-2, approaches of targeting antigens and engineered Tregs. Investigating the areas of stage and compartment-specific CD4 T-cell circuits can help to advance targeted immunomodulation in progressive MS and neuro-repair. - Source: PubMed
Publication date: 2026/06/25
Egba Simeon IkechukwuIkechukwu Gavin ChibunduOkereke Chinenye IheanyiOrhonigbe Innocent OgheneovoUroko Robert IkechukwuUgwu Okechukwu Paul Chima - 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