Human Interleukin 5,IL-5 ELISA KIT
- Known as:
- Human Interleukin 5,Interleukin-5 Enzyme-linked immunosorbent assay test KIT
- Catalog number:
- 201-12-0092
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 5 IL-5 ELISA KIT
Ask about this productRelated genes to: Human Interleukin 5,IL-5 ELISA KIT
- 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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Related articles to: Human Interleukin 5,IL-5 ELISA KIT
- 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
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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
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