Monkey IL-5 ELISPOT kit, enzymatic staining
- Known as:
- Monkey Interleukin-5 ELISPOT reagent, enzymatic staining
- Catalog number:
- ct129-pr2
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- U-CyTech biosciences
- Gene target:
- Monkey IL-5 ELISPOT kit enzymatic staining
Related genes to: Monkey IL-5 ELISPOT kit, enzymatic 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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- This review addresses the growing understanding that a specific subset of patients with a respiratory disease, including asthma, chronic obstructive pulmonary disease (COPD), or bronchiectasis may have one thing in common: type 2 inflammation. In the era of personalized medicine, we need to refine clinical markers combined with molecular and cellular endotyping to improve patient outcomes. - Source: PubMed
Publication date: 2025/03/19
Schedel MichaelaHeimel VictoriaTaube Christian - Prurigo nodularis (PN) is a chronic inflammatory skin disorder characterized by intensely pruritic nodules. The pathogenesis of PN involves immune dysregulation, with a predominance of T helper (Th2)-type inflammation, including interleukin (IL)-4, IL-5, IL-13, and IL-31. Nemolizumab, an IL-31 receptor A inhibitor, was newly approved for PN in 2024. We report a case of erythema multiforme (EM) that developed three weeks after the first administration of nemolizumab. Three weeks post-injection, she developed multiple targetoid edematous erythematous patches and plaques on her trunk and limbs, leading to a clinical diagnosis of EM. Since she had no new medications and no recent history of infections, we inferred that the development of EM was likely associated with the administration of nemolizumab. The pathophysiology of EM involves a predominant Th1-driven inflammatory response. Therefore, nemolizumab likely suppressed Th2 inflammation, leading to compensatory Th1 hyperactivation, which may have triggered EM. To our knowledge, this may be the first reported case of EM following nemolizumab treatment for PN. Further research is necessary to investigate its immunomodulatory effects and potential adverse events. - Source: PubMed
Publication date: 2025/02/15
Mima YoshihitoOhtsuka Tsutomu - Asthma is a chronic inflammatory disease characterized by dysregulated cytokine expression. The RNA-binding protein KSRP reduces the expression of several pro-inflammatory mediators. Therefore, we investigated whether KSRP modulates Th2-associated immune responses in vivo in an ovalbumin-induced (OVA) allergic asthma model in C57BL/6 KSRP-deficient mice (KSRP). - Source: PubMed
Publication date: 2025/03/17
Palzer Kim-AliciaBolduan VanessaLakus JelenaTubbe IngridMontermann EvelynClausen Björn EBros MatthiasPautz Andrea - -acetylcysteine (NAC) is a classical mucolytic agent that, in addition to its mucolytic activity, also exhibits antioxidant activity. This could be beneficial in treating chronic inflammatory airway diseases, including asthma. We evaluated the ability of NAC to modulate airway defense mechanisms, airway reactivity, inflammation, and remodeling after 10 days of administration [20 and 60 mg/(kg·d)] in an experimental guinea pig model of allergic inflammation. The concentrations of inflammatory cytokines (interleukins: IL-4, IL-5, IL-10, IL-12, and IL-13), granulocyte macrophage-colony stimulating factor (GM-CSF), interferon-gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) were measured in bronchoalveolar lavage fluid using a multiplex detection method. The concentration of remodeling marker transforming growth factor beta-1 (TGF-β1) was measured in lung homogenates using enzyme-linked immunosorbent assay. changes in specific airway resistance and number of cough efforts were determined. Tracheal smooth muscle reactivity was evaluated . Ciliary beat frequency (CBF) indicated mucociliary clearance. A 10-day administration of NAC at a higher dosage led to a significant decrease in the regulatory cytokines IL-4, IL-5, and GM-CSF. NAC, in both dosing schedules, decreased the levels of TGF-β1. NAC at a higher dosage reduced the number of chemically induced cough reflexes and CBF. NAC did not affect airway hyperreactivity parameters. NAC is a multifactorial drug, and under our experimental conditions of allergic inflammation, it showed positive effects on the levels of regulatory cytokines and growth factors, which probably led to a reduction in the intensity of airway defense mechanisms. - Source: PubMed
Publication date: 2025/03/17
Smieško LukášMažerik JozefGondáš EduardDohál MatúšJošková MartaŠutovská MartinaFraňová Soňa - Eosinophils are immune cells that are crucial for the pathogenesis of allergic diseases, such as asthma. These cells play multifunctional roles in various situations, including infection. They are activated during viral infections and exert antiviral activity. Pattern recognition receptors, toll-like receptor 7 and retinoic acid inducible gene-I, are important for the recognition and capture of RNA viruses. In addition, intracellular granule proteins (eosinophil cationic protein and eosinophil-derived neurotoxin) and intracellular nitric oxide production inactivate and/or degrade RNA viruses. Interestingly, eosinophil-synthesizing specialized pro-resolving mediators possess antiviral properties that inhibit viral replication. Thus, eosinophils may play a protective role during respiratory virus infections. Notably, antiviral activities are impaired in patients with asthma, and eosinophil activities are perturbed in proportion with the severity of asthma. The exact roles of eosinophils in RNA virus (rhinovirus, respiratory syncytial virus, and influenza virus)-induced type 2 inflammation-based asthma exacerbation remain unclear. Our research demonstrates that interferons (IFN-α and IFN-γ) stimulate human eosinophils to upregulate antiviral molecules, including guanylate-binding proteins and tripartite motifs. Furthermore, IFN-γ specifically increases the expression of IL5RA, ICAM-1, and FCGR1A, potentially enhancing cellular responsiveness to IL-5, ICAM-1-mediated adhesion to rhinoviruses, and IgG-induced inflammatory responses, respectively. In this review, we have summarized the relationship between viral infections and asthma and the mechanisms underlying the development of antiviral functions of human and mouse eosinophils and . - Source: PubMed
Publication date: 2025/02/28
Sasaki HisashiMiyata JunKawana AkihikoFukunaga Koichi