TNF-alpha IHC Antibody
- Known as:
- TNF-a Immunohistochemistry Antibody
- Catalog number:
- IW-PA1079
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- IHC
- Gene target:
- TNF-alpha IHC Antibody
Related products to: TNF-alpha IHC Antibody
Related articles to: TNF-alpha IHC Antibody
- Breast cancer (BC), characterized by a high incidence specifically in women, exhibits a complex etiology. This study aims to investigate the role and underlying mechanism of microrchidia CW-type zinc finger 2 (MORC2) in BC progression. MCF-7 and MDA-MB-231 cells with MORC2 knockdown were utilized to investigate the impact of MORC2 on BC. To explore the in vivo functions of MORC2, xenograft tumor mouse model was established. In this study, we discovered that MORC2 was significantly upregulated in BC tumor tissues. Consistent with MORC2 functioning as a suppressor of pyroptosis, MORC2 knockdown enhanced the expression of pyroptosis-related markers (Caspase-1, NLRP3, GSDMD-N, and LDH) and inflammatory factors (IL-18, IL-1β, and TNF-α), while suppressing CCL5, CCL2 levels, and macrophage migration. Furthermore, MORC2 knockdown inhibited tumor growth in vivo, decreased CD68 cell infiltration and M2 markers, and increased the M1/M2 macrophage ratio. TAMs from MORC2-knockdown tumors exhibited reduced immunosuppressive capacity, promoting T cell proliferation and IFN-γ/IL-2 production. Mechanistically, silencing of MORC2 suppressed the Wnt/β-catenin pathway, and Compound 3 f significantly reversed the effects of MORC2 knockdown on pyroptosis and macrophage recruitment BC. In summary, MORC2 suppresses pyroptosis and promotes TAMs recruitment in BC; MORC2 knockdown alleviated the progression of BC by reversing these effects, which was mediated by suppressing the Wnt/β-catenin signaling pathway. - Source: PubMed
Liu ZhiyongHu HongLin ZhiqinMeng Xiaoshan - Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are characterized by lipid accumulation, inflammation, and fibrosis. Existing preclinical models often fail to capture multicellular interactions that shape disease progression. In this study, we established a human multicellular 3D liver spheroid model comprising HepaRG hepatocytes, hepatic stellate cells, liver sinusoidal endothelial cells, and Kupffer cells. Spheroids were analyzed for lipid accumulation, cytokine secretion, hepatocellular injury, and extracellular matrix remodeling using immunofluorescence, qPCR, ELISA, and LDH release assays. The model exhibited multicellular spatial organization resembling the native liver microarchitecture. Lipid accumulation was most pronounced under MASLD conditions, whereas progression to MASH was associated with stronger inflammatory and fibrosis-related changes. TNF-α showed the clearest Kupffer cell-associated increase, whereas IL-6 changes were less consistent and likely reflected the broader inflammatory response of a multicellular system. LDH release increased with disease severity and was most pronounced in MASH without evidence of a robust Kupffer cell-specific effect. Fibrotic remodeling was reflected by increased expression of fibronectin, collagen III, and procollagen I. Together, these findings establish a human multicellular in vitro platform that recapitulates the key disease-relevant features of MASLD/MASH under controlled conditions. - Source: PubMed
Publication date: 2026/05/18
Bogovic NiklasDrießlein MariaKeller MarieSchlitt Hans JGeissler Edward KSchneider LydiaKreiner PhilippJunger HenrikEggenhofer Elke - Lung cancer remains the leading cause of cancer-related mortality, with poor outcomes driven by late presentation and therapy resistance. Although genes encoding secreted proteins may reflect tumor biology and have biomarker potential, systematic multi-cohort studies identifying and validating prognostically relevant secreted-protein candidates in non-small cell lung cancer (NSCLC) are limited. - Source: PubMed
Publication date: 2026/05/18
Kim JoonLee GeuninYong Seung-HyunKim Eun YoungJo YunjuJeong WoojuRyu DongryeolOh Chang-MyungLee Sang Hoon - The role of systemic therapy in paediatric Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) remains undefined. Management is primarily guided by observational data and variable practice patterns. This systematic review aims to integrate recent evidence and evaluate clinical outcomes associated with systemic therapies in paediatric SJS/TEN. - Source: PubMed
Publication date: 2026/05/17
Ting SamanthaChua Kangjie ReuelWong Li-ChuenFong Gloria - Trypanosoma cruzi infection, which causes Chagas' disease, induces an immune response in the host whose efficiency is important for the infection to persist or be eliminated. Alcohol consumption produces a great impact on the immune system, inducing alterations in the determination of T lymphocyte effector function, directing the profile of these cells to tolerance or inflammation. Our study aimed to evaluate, in C57BL/6 mice, the cytokine production in splenic leukocytes from T. cruzi infected and treated (EtOH) for 15 days and controls. Twenty-four mice were randomised into four groups, with 12 animals each: (1) Non-Infected Control (NI), (2) Control Infected (CI), (3) Experimental Non-Infected (EtOHNI), and (4) Experimental Infected (EtOH-I). Ethanol-pre-exposed infected mice exhibited elevated parasitaemia during the patent period compared to controls. Adaptive immunity was characterised by increased IL-4, IL-10 and IFN-γ production by CD8+ T lymphocytes, while innate immunity showed reduced cytokine production, particularly in NK cells and macrophages. Ethanol amplified IL-10 and IFN-γ responses in macrophages yet suppressed TNF-α production in dendritic cells and macrophages during infection. These findings suggest ethanol modulates the immune response by enhancing adaptive immunity while impairing innate mechanisms, contributing to altered host-pathogen dynamics in T. cruzi infection. - Source: PubMed
Moura Paulo Henrique TolentinoNoronha Beatriz PradoAraujo Marcio Sobreira SilvaMoreira Marcela LimaLopes Diego Patrick Soaresde Oliveira Rodrigo Gentil Miquilinode Paula Junior WaldemarAndrade Marileia Chaves