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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- Severe asthma affects a minority of patients but accounts for disproportionate morbidity, mortality, and healthcare costs. The development of targeted biologic therapies has revolutionized treatment, offering precision medicine approaches based on underlying inflammatory endotypes. Currently approved biologics target immunoglobulin E (omalizumab), interleukin (IL)-5 or its receptor (mepolizumab, reslizumab, depemokimab, and benralizumab), IL-4 receptor α (dupilumab), and thymic stromal lymphopoietin (tezepelumab). These agents have demonstrated substantial reductions in exacerbation rates, improved lung function, corticosteroid-sparing effects, and enhanced quality of life across diverse patient populations. This review examines the mechanisms of action, clinical efficacy, safety profiles, and optimal patient selection strategies for biologic therapies in severe asthma and eosinophilic COPD. - Source: PubMed
Publication date: 2026/06/01
Hemachandra ShanNgu Jia LiGoutama Evan NOoi Horng ChenAngel AngelEi Cho TheintGoh EvaAung Arkar MInayah Ruby SKoo Kai Jie AnselmGaur Nisha - Eosinophils amplify type-2 (Th2) inflammation and tissue injury in allergic rhinitis (AR), and eosinophilic burden correlates with disease severity and future asthma risk. Current AR therapies have limitations, motivating interest in non-pharmacologic neuromodulatory approaches. Here, we tested whether electroacupuncture (EA) attenuates eosinophilic inflammation in AR and probed a candidate neuroimmune mechanism. - Source: PubMed
Publication date: 2026/06/16
Quach Tran Van BaoNguyen Thanh-Hien VuNguyen Ngoc Chi LanLin Che-HsuanChen Yi-Hung - Cytotoxic type 2 T cells (Tc2) are increasingly recognized as contributors to type 2 inflammation, including asthma, yet the metabolic programs that support their function remain poorly defined. We aimed to define the metabolic requirements of Tc2 cells, identify pathways that regulate their effector function, and assess whether serotonin-modifying therapies are associated with altered Tc2 responses and allergic sensitization in humans. - Source: PubMed
Publication date: 2026/07/01
de Souza Ferreira SabrinaHolla LisaBjörkander SophiaBek Marie KaarupWirth LorenzShearer Patrick ASäfholm JesperSachs ErikAl-Ameri MamdohVali KasraEkström SandraMelén ErikMjösberg JennyTibbitt Christopher Andrew - Asthma, COPD, and ACO are chronic airway disorders with distinct and overlapping features. This study aimed to compare clinical profiles, inflammatory biomarkers, and quality of life among these groups. - Source: PubMed
Publication date: 2026/06/24
Safwan M AhmedGoel NitinKumar Raj - Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease that is entering a new era in precision medicine. Advances in disease endotyping have challenged the traditional view of COPD as a uniformly neutrophilic disorder and revealed biologically distinct subgroups in whom targeted immunomodulation may be effective. Reproducible signatures of type 2 (T2) inflammation and epithelial-derived alarmin activation have emerged as actionable pathways, reshaping therapeutic development in COPD. This narrative review synthesises mechanistic insights and clinical trial evidence for biologic therapies targeting key T2 cytokines such as interleukin-5 (IL-5) IL-4/IL-13 and upstream epithelial alarmins, including interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP). We examine why earlier approaches targeting neutrophilic inflammation failed, and how biomarker-driven trial design has enabled success in selected populations. Across these programmes, therapeutic efficacy has depended not only on the pathway targeted but also on patient selection, disease stage and timing of intervention. We propose that the future of biologics in COPD lies in integrating biomarkers, treatable traits and longitudinal phenotyping to align the right patient with the right pathway at the right time, closing persistent treatment gaps in this common, overlooked and burdensome disease. - Source: PubMed
Publication date: 2026/06/29
Finney Lydia JConway Francesca MSethi Dheeraj K