Chimpanzee IL-5 ELISPOT kit, silver staining
- Known as:
- Chimpanzee Interleukin-5 ELISPOT reagent, silver staining
- Catalog number:
- ct173-pb5
- 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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- BackgroundSystemic inflammation has been implicated in cognitive aging and neurodegeneration; however, inflammatory biomarkers are expressed in coordinated patterns rather than as isolated markers.ObjectiveTo identify latent inflammatory biomarker groupings and evaluate their associations with cognitive performance among midlife and older adults.MethodsThis cross-sectional study included 334 participants from the Aging Research Characterizing Health Exposome via Social Drivers (ARCHES) study. Cognitive performance was assessed using the Preclinical Alzheimer Cognitive Composite (PACC). Plasma inflammatory biomarkers were quantified using the NuLISA™ multiplex immunoassay platform. Exploratory factor analysis (EFA) (minimum residual extraction, oblimin rotation) identified latent inflammatory factors, retaining biomarkers with loadings ≥0.40. Factor scores were evaluated in multivariable linear regression models adjusted for age, sex, education, and genotype status; sensitivity analyses adjusted for socioeconomic context, medication use, BMI, lifestyle factors, and clinical diagnoses. Age-stratified and nonlinear spline analyses were conducted.Results27 of 43 biomarkers formed an eight-factor structure explaining 43% of variance. Two factors were significantly associated with cognitive performance after FDR correction. Factor 4 (CCL4, CXCL1, S100A12) and Factor 5 (IL2, IL5, IL13, IL10, CSF2) were inversely associated with PACC scores. These associations remained consistent across sensitivity analyses. Age-stratified analyses showed that several inflammatory factors were associated with cognitive performance among participants aged 45-<65 years, whereas no factors remained significant among participants aged ≥65 years after FDR correction. Nonlinear modeling indicated a non-linear age-cognitive performance relationship.ConclusionsEFA identified clusters of correlated inflammatory biomarkers associated with cognitive performance in this cohort of midlife and older adults. - Source: PubMed
Publication date: 2026/09/02
Singh Ramkrishna KBekena SemereWalker Alexis I BTaylor KaylinZhu YiqiPal SubrataMohamed Essa ATrani Jean-FrancoisKaplan IanBabulal Ganesh M - Asthma is a chronic inflammatory airway disease characterized by Th2- dominant immune responses, airway hyperresponsiveness, and structural remodeling. Although inhaled corticosteroids and biologics are effective for many patients, a substantial proportion remains poorly controlled and experiences treatment-related adverse effects. Probiotics have emerged as immunomodulatory agents in asthma, but existing studies predominantly focus on oral administration and gut-lung axis regulation. Whether direct respiratory administration of probiotics can modulate the pulmonary immune microenvironment and alleviate asthma remains largely unexplored. - Source: PubMed
Publication date: 2026/09/01
Yang XinYu FanWu XiaochengLi ShuxianWang YingshuoHu ZhongXie YichengMa DaqingWu Lei - Type 2 inflammation is a fundamental immunologic pathway underlying a growing spectrum of dermatologic diseases. While classically associated with atopic dermatitis, type 2 immune responses are increasingly recognized as key contributors to prurigo nodularis, chronic spontaneous urticaria, bullous pemphigoid, lichen simplex chronicus, and other chronic pruritic disorders. Barrier disruption and epithelial injury initiate the release of alarmins, including thymic stromal lymphopoietin (TSLP), interleukin (IL)-33, and IL-25, which activate innate and adaptive immune pathways that promote type 2 inflammation. Subsequent production of effector mediators such as IL-4, IL-13, IL-5, IL-31, immunoglobulin E (IgE), and periostin drives barrier dysfunction, immune cell recruitment, tissue remodeling, and chronic pruritus. Increasing evidence further highlights the importance of neuroimmune crosstalk, with direct interactions between immune cells, cytokines, and sensory neurons contributing to itch sensitization and disease persistence. The clinical success of biologic therapies targeting IL-4/IL-13, IgE, and IL-31 signaling has provided powerful functional validation of these pathogenic pathways and has transformed the management of multiple inflammatory skin diseases. In this review, we summarize the molecular and cellular mechanisms underlying type 2 inflammation in the skin, discuss its role across diverse dermatologic conditions, and highlight emerging concepts in disease heterogeneity, neuroimmune signaling, and precision medicine. Collectively, these findings support type 2 inflammation as a unifying immunologic framework and therapeutically actionable target across dermatology. - Source: PubMed
Publication date: 2026/08/17
Khalil NicoleFarhadi LeahYosipovitch Gil - Allergic rhinitis (AR) is a common chronic inflammatory disorder characterized by nasal mucosal inflammation, sneezing, and rhinorrhea. Schisandrin A (Schis-A) has demonstrated significant anti-inflammatory effects in models of allergic asthma. This study aimed to evaluate the therapeutic efficacy of Schis-A in AR and to elucidate its underlying molecular mechanisms. An AR mouse model was established by sensitization and challenge with ovalbumin (OVA), followed by oral administration of Schis-A at doses of 40 and 80 mg/kg/day. Nasal symptoms were monitored and quantified. OVA-specific immunoglobulin E (IgE) levels and T helper (Th)1/Th2- and regulatory T cells (Treg)/Th17-associated cytokines were measured using enzyme-linked immunosorbent assay and quantitative real-time PCR. Treg and Th17 cell populations were analyzed by flow cytometry. The results showed that Schis-A treatment significantly reduced OVA-induced nasal rubbing and sneezing, indicating effective attenuation of allergic responses. Serum OVA-specific IgE levels were markedly reduced in Schis-A-treated AR mice. Moreover, Schis-A restored Th1/Th2 and Treg/Th17 cytokine balance, as indicated by upregulated expression of IFN-γ, IL-2, and Foxp3, alongside downregulation of IL-4, IL-5, IL-13, and IL-17. Flow cytometric analysis confirmed an increase in Treg cells and a reduction in Th17 cell populations. Mechanistically, Schis-A inhibited activation of the PI3K/AKT signaling pathway, suggesting that this pathway may contribute to its immunomodulatory effects. Schis-A alleviates AR by modulating Th1/Th2 and Treg/Th17 immune responses and inhibiting PI3K/AKT pathway activation, offering a promising therapeutic strategy for the treatment of AR. - Source: PubMed
Publication date: 2026/08/25
Zhang ZhipengHe ShanYu YanminDeng YongjunChen YuanGu XiaoyiQiu XiaoyiWei JingjingShi YanJiao Yu - Inflammation is a common pathway in acute or chronic cardiac injury. This study aimed to explore the characteristics of systemic inflammatory responses in acute myocardial infarction (AMI) and find the key inflammatory factors in the prognosis of AMI patients. - Source: PubMed
Publication date: 2026/08/26
Cao WenMeng LiyeWu XiaojuanYang LangchengGan WeiFeng WeihuaZhang JunlongCai Bei