Chimpanzee IL-5 ELISPOT kit, silver staining
- Known as:
- Chimpanzee Interleukin-5 ELISPOT reagent, silver staining
- Catalog number:
- ct173-t2
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Chimpanzee IL-5 ELISPOT kit silver staining
Related genes to: Chimpanzee IL-5 ELISPOT kit, silver staining
- Gene:
- CSF2RB NIH gene
- Name:
- colony stimulating factor 2 receptor beta common subunit
- Previous symbol:
- IL3RB
- Synonyms:
- IL5RB, CD131, betaGMR
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2017-07-12
- Gene:
- IL5 NIH gene
- Name:
- interleukin 5
- Previous symbol:
- -
- Synonyms:
- IL-5, EDF, TRF
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-07-06
- Gene:
- IL5RA NIH gene
- Name:
- interleukin 5 receptor subunit alpha
- Previous symbol:
- IL5R
- Synonyms:
- CDw125, CD125
- Chromosome:
- 3p26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-18
- Date modifiied:
- 2016-10-11
- Gene:
- LRR1 NIH gene
- Name:
- leucine rich repeat protein 1
- Previous symbol:
- PPIL5
- Synonyms:
- MGC20689, LRR-1
- Chromosome:
- 14q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-20
- Date modifiied:
- 2014-11-18
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- positive chronic eosinophilic leukemia (CEL) is a rare subtype of myeloproliferative neoplasm characterized by organ damage caused by eosinophilic granules containing cytokines and humoral factors. These include interleukin-5 (IL-5), interleukin-4 (IL-4), and interleukin-13 (IL-13). We present a case study of a 71-year-old male who initially presented with cough, fever, night sweats, and weight loss. Fluorescence in situ hybridization (FISH) and cytogenetic testing confirmed that the patient had positive chronic eosinophilic leukemia. Treatment with imatinib and prednisone led to a rapid decrease in the eosinophil count without further damage from eosinophilic infiltration. Our patient has tolerated therapy with occasional lightheadedness that he attributed to external factors, and he continues to remain in remission. This case study aims to contribute to the existing knowledge regarding the discovery and treatment of this disease. - Source: PubMed
Publication date: 2025/02/24
Haydon Steven JRoss Danielle ECaucci StephenClark ShaneHrinczenko Borys - Space flight exposes astronauts to stressors that alter the immune response, rendering them vulnerable to infections and diseases. In this study, we aimed to determine the levels of inflammasome activation in the brains of mice that were housed in the International Space Station (ISS) for 37 days. C57BL/6 mice were launched to the ISS as part of NASA's Rodent Research 1 Mission on SpaceX-4 CRS-4 Dragon cargo spacecraft from 21 September 2014 to 25 October 2014. Dissected mouse brains from that mission were analyzed by immunoblotting of inflammasome signaling proteins and Electrochemiluminescence Immunoassay (ECLIA) for inflammatory cytokine levels. Our data indicate decreased inflammasome activation in the brains of mice that were housed in the ISS for 37 days when compared to the brains of mice that were maintained on the ground, and in mice corresponding to the baseline group that were sacrificed at the time of launching of SpaceX-4. Moreover, we did not detect any significant changes in the expression levels of the pro-inflammatory cytokines TNF-α, IL-2, IFN-γ, IL-5, IL-6, IL-12p70 and IL-10 between the ground control and the flight groups. Together, these studies suggest that spaceflight results in a decrease in the levels of innate immune signaling molecules that govern inflammasome signaling in the brain of mice. - Source: PubMed
Publication date: 2025/03/12
Roy UpalHadad RoeyRodriguez Angel ASaju AlenRoy DeepaGil MarioKeane Robert WScott Ryan TMao Xiao Wde Rivero Vaccari Juan Pablo - (1) Background: Despite previous studies linking inflammatory cytokines to lung adenocarcinoma (LUAD), their causal mechanisms remain unclear. This study aims to explore the causal relationship between inflammatory cytokines and LUAD to fill this knowledge gap. (2) Methods: This study employs a comprehensive approach, integrating Mendelian randomization (MR) analysis, single-cell RNA sequencing (scRNA-seq), and transcriptomic sequencing (RNA-seq) data to investigate the relationship between inflammatory cytokines and LUAD. (3) Results: In forward MR analysis, elevated levels of hepatocyte growth factor (HGF), interleukin-1 receptor antagonist (IL-1RA), IL-5, monocyte chemoattractant protein-3, and monokine induced by interferon-γ were causally associated with an increased risk of LUAD. In reverse MR analysis, LUAD exhibited a positive causal relationship with the levels of regulated upon activation normal T cell expressed and secreted factor (RANTES) and stromal cell-derived factor-1α. The scRNA-seq data further identified specific cell populations that may influence LUAD onset and progression through the expression of particular inflammatory genes and intercellular communication. RNA-seq data analysis highlighted the role of the HGF gene in LUAD diagnosis, demonstrating its strong correlation with patient prognosis and immune cell infiltration within the tumor microenvironment. (4) Conclusions: The findings reveal a causal relationship between inflammatory cytokines and LUAD, with HGF emerging as a potential biomarker of significant clinical relevance. This study provides new insights into the molecular mechanisms underlying LUAD and lays the foundation for future therapeutic strategies. - Source: PubMed
Publication date: 2025/03/19
Sun MengxuanYu YangZhu HanciYao YanZhou XintongWang XueZhang YubaoXu XiaoweiZhuang JingSun Changgang - The role of eosinophils in COPD and their utility as biomarkers for cytokine targeting monoclonal therapies remains unclear. We investigated the distribution of eosinophils across different tissue compartments in COPD and analysed gene expression to understand the possible mechanistic drivers of eosinophilic inflammation in COPD. - Source: PubMed
Publication date: 2025/03/25
Staples Karl JAckland JodieLukose SruthymolAngermann BastianBelfield GrahamBelvisi MariaChaerkady RaghothamaEtal DamlaHeinson AshleyHess SonjaHristova Ventzislava AHühn MichaelMcCrae ChristopherMuthas DanielÖberg LisaOstridge KristofferPlatt AdamSpalluto C MirellaWatson AlastairWilkinson Tom - Type 2 inflammatory diseases are common in cystic fibrosis (CF) including asthma, sinusitis, and allergic bronchopulmonary aspergillosis. CD4+ T helper 2 (Th2) cells promote these diseases through secretion of IL-4, IL-5, and IL-13. Whether the cystic fibrosis transmembrane conductance regulator (CFTR), the mutated protein in CF, has a direct effect on Th2 development is unknown. Using murine models of CFTR deficiency and human CD4+ T cells, we show CD4+ T cells expressed Cftr transcript and CFTR protein following activation. Loss of T cell CFTR expression increased Th2 cytokine production compared to control cells. Mice with CFTR-deficient T cells developed increased allergic airway disease to Alternaria alternata extract compared to control mice. Culture of CFTR-deficient Th2 cells demonstrated increased IL-4Rα expression and increased sensitivity to IL-4 with greater induction of GATA3 and IL-13 compared to control Th2 cell cultures. The CFTR potentiator ivacaftor reduced allergic inflammation and type 2 cytokine secretion in bronchoalveolar lavage of "humanized" CFTR mice following Alternaria alternata extract challenge and decreased Th2 development in human T cell culture. Together, these data support a direct role of CFTR in regulating T cell sensitivity to IL-4 and demonstrate a potential CFTR-specific therapeutic strategy for Th2 cell-mediated allergic disease. - Source: PubMed
Publication date: 2025/03/25
Rusznak MarkThomas Christopher MZhang JianToki ShinjiZhou WeisongAbney MasakoYanda Danielle MNorlander Allison EHodges Craig ANewcomb Dawn CKaplan Mark HPeebles R StokesCook Daniel P