Cymax Human IL-5 ELISA Kit
- Known as:
- Cymax Human Interleukin-5 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0259
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Human IL-5 ELISA Kit
Related genes to: Cymax Human 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
Related products to: Cymax Human IL-5 ELISA Kit
Related articles to: Cymax Human IL-5 ELISA Kit
- Mepolizumab, an anti-IL5 monoclonal antibody, effectively reduces exacerbations and improves disease control in severe eosinophilic asthma (SEA). While this treatment rapidly decreases blood eosinophil counts, some patients continue to experience asthma symptoms, suggesting that other features beyond eosinophil number contribute to disease persistence. In this work, we aim to characterize the molecular and functional signature of circulating eosinophils in SEA in response to mepolizumab therapy. - Source: PubMed
Publication date: 2026/08/26
Miguéns-Suárez PabloVázquez-Mera SaraMartelo-Vidal LauraAparicio Marina BlancoÁlvarez Uxío CalvoFernández Coral GonzálezAñón Mar MosteiroAbelaira Dolores CorbachoValverde Tamara HermidaHenríquez Christian CalvoBravo Susana BUller LenaNieto-Fontarigo Juan JSalgado Francisco JGonzález-Barcala Francisco J - Differentiating active ulcerative colitis (UC) from Crohn's disease (CD) is one of the unmet needs addressed by biomarkers in inflammatory bowel disease (IBD). The immune landscapes of UC and CD differ, justifying the search for discriminatory markers and novel therapy targets among their mediators. Herein, 27 systemic cytokines were measured using flow cytometry-based methodology in 138 IBD patients, with an additional 21 being determined in 67 of the patients. Their discriminatory power was assessed individually and as exploratory multivariable signatures generated using logistic regression, hierarchical clustering, and principal component analysis. Eotaxin-1, macrophage inflammatory protein (MIP)-1β, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) showed fair discriminatory potential, while multivariable models performed better. Interleukin (IL)-1β, IL-4, and MIP-1α were strongly associated with CD, whereas IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), MIP-1β, and TRAIL were associated with UC. Active UC was characterized by mediators linked to eosinophil-, mastocyte-, and neutrophil-driven inflammation and tissue repair (eotaxin-1, IL-5, growth-regulated oncogene (GRO), MIP-1β, stem cell factor (SCF), GM-CSF, IL-1 receptor antagonist, TRAIL, stem cell growth factor (SCGF)-β, and cutaneous T cell-attracting chemokine (CTACK)), whereas active CD was associated with Th1/Th17 immunity, myeloid activation, fibrosis, angiogenesis, and neuroimmune remodeling (IL-1β, IL-12p70, IL-15, 'regulated on activation, normal T-cell expressed and secreted' (RANTES), MIP-1α, stromal cell-derived factor (SDF)-1α, nerve growth factor β (β-NGF), and leukemia inhibitory factor (LIF)). In conclusion, integrated circulating immune signatures identify several understudied cytokines as potential contributors to disease-specific pathways and show potential in distinguishing active UC from CD warranting further mechanistic studies and independent validation in larger cohorts. - Source: PubMed
Publication date: 2026/08/13
Krzystek-Korpacka MałgorzataLewandowski ŁukaszBednarz-Misa IwonaKorpacki AndrzejNeubauer Katarzyna - Staphylococcus aureus frequently colonizes the skin and upper airways and produces a broad repertoire of immunomodulatory molecules. In asthma, the most consistent evidence concerns staphylococcal enterotoxins (SEs), which can act both as superantigens and as allergens, and IgE sensitization to SEs (SE-sIgE). SE-sIgE is associated with severe asthma, type 2 inflammation, chronic rhinosinusitis with nasal polyps (CRSwNP), exacerbations, and, in some longitudinal studies, persistent airflow obstruction. However, this relationship is not necessarily causal: SE-sIgE may reflect exposure, an immune response, or a biologically active endotype, whereas colonization, local toxin production, and systemic sensitization are not equivalent. SEs simultaneously bind class II MHC molecules and Vbeta regions of the T-cell receptor, activating large fractions of T lymphocytes; they also promote IL-4, IL-5, and IL-13 production, polyclonal B-cell activation, local IgE synthesis, mast-cell degranulation, eosinophilia, and IL-8/neutrophil circuits. Alpha-toxin (Hla) and SEB can damage the epithelial barrier, facilitating allergen penetration and alarmin signalling. These observations support an interaction model in which dysbiosis, barrier dysfunction, and type 2 immunity mutually reinforce one another along the nasobronchial axis. Corticosteroids and antibiotics may modify selected nodes in this circuit, but current evidence is insufficient to recommend decolonization or antitoxin therapy in stable asthma. Biologics interrupt downstream pathways potentially fuelled by toxins: omalizumab neutralizes free IgE; mepolizumab and benralizumab reduce the eosinophilic axis; dupilumab blocks IL-4/IL-13 signalling; and tezepelumab acts upstream on TSLP. Nevertheless, randomized trials stratified by SE-sIgE are lacking, and no evidence demonstrates that these treatments eliminate colonization or toxin production. SE-sIgE therefore appears to be a promising biomarker, particularly in severe asthma with CRSwNP, but it is not yet an autonomous criterion for biologic selection. A broader barrier-organ analysis also identifies nasal, cutaneous, and intestinal colonization as distinct ecological states; atopic dermatitis as a complementary model of toxin-amplified type 2 inflammation; and biofilms and extracellular vesicles as candidate mechanisms of persistent toxin delivery. These data increase biological plausibility but remain indirect for asthma. - Source: PubMed
Publication date: 2026/07/23
Bagnasco DiegoBondi BenedettaLosacco GretaMontagnino CarolaFroio FrancescaTedesco ElenaD'Alessandro GloriaBaglivo IlariaBruno LauraChiappori SaraMurillo Jaramillo Maria JoséMincarini MarcelloBraido FulvioCaruso Cristiano - Waning immunity after primary COVID-19 vaccination supports evaluation of additional doses. HXP-GPOVac is an egg-based, inactivated Newcastle disease virus (NDV)-vectored vaccine expressing a prefusion-stabilized SARS-CoV-2 HexaPro spike antigen. We evaluated the safety, tolerability, and immunogenicity of a single additional 10 µg dose of HXP-GPOVac administered to adults previously primed with two doses of either HXP-GPOVac or BNT162b2. Study GPO NDV-HXP-S 203 was an open-label phase II extension enrolling adults (18-75 years) who previously completed a two-dose primary series in Study 202 with either HXP-GPOVac or BNT162b2 (Pfizer-BioNTech; Comirnaty). All participants received a single additional 10 µg intramuscular dose of HXP-GPOVac ≥ 6 months after their second primary dose. Solicited local/systemic adverse events (AEs) were recorded for 7 days, unsolicited AEs through Day 28, and serious AEs (SAEs) and adverse events of special interest (AESIs) throughout follow-up. Neutralizing antibody titers (pseudovirus 50% neutralization titer, NT) and anti-spike IgG (BAU/mL) were assessed pre-dose (Day 1) and post-vaccination through 12 months; a predefined subset underwent IFN-γ and IL-5 ELISpot. SARS-CoV-2 infection during follow-up was assessed using anti-nucleocapsid (anti-N) IgG. Symptomatic COVID-19 was identified through symptom-reported, symptom-triggered RT-PCR testing; sequencing was performed when feasible. All 219 participants received HXP-GPOVac (167 primed with HXP-GPOVac and 52 with BNT162b2). Any solicited local reaction occurred in 22.2% (37/167) of HXP-GPOVac-primed and 26.9% (14/52) of BNT162b2-primed participants; any solicited systemic reaction occurred in 10.8% (18/167) and 13.5% (7/52), respectively. No vaccine-related unsolicited AEs or AESIs were reported. Three deaths occurred during the 12-month follow-up; one (a sudden cardiac death in an HXP-GPOVac-primed participant) was assessed by the safety medical team as possibly related to vaccination, and two were assessed as not related. Neutralizing antibody GMTs increased from 46.33 at baseline to 1569.04 at Day 15 in HXP-GPOVac-primed participants and from 77.25 to 841.34 in BNT162b2-primed participants; corresponding SCRs were 78.8% and 76.9%. Anti-spike IgG GMCs increased from 48.79 to 1480.14 BAU/mL and from 194.48 to 1547.88 BAU/mL, respectively. Responses declined over time but remained above baseline through 12 months. In the cellular immunity subset, post-vaccination IFN-γ responses increased, with comparatively modest IL-5 responses and no pattern suggestive of Th2 predominance. A single additional dose of HXP-GPOVac administered ≥6 months after primary vaccination with HXP-GPOVac or BNT162b2 was generally well tolerated and elicited robust recall humoral responses, with supportive findings of cellular immunity. Trial registration: Thai Clinical Trials Registry, TCTR20230213001. - Source: PubMed
Publication date: 2026/07/28
Praphasiri PrabdaDitsungneon DaruneeKerdsin AnusakNakphook SutthichaiKittiwatanachod JiraphutSornwong KanlayaNaosri SuriyaKhunarsa SarunpattoriWirachwong PonthipTechatanawat IsariyaNarakorn PiengthongSurichan SomchaiyaFlores JorgeMercer Laina DPolyak Christina SInnis Bruce LRaghunandan RamaPittayawonganon ChakraratIamsirithaworn SoponSirilak SupakitPrasert Kriengkrai - Type 2 CD8 T (Tc2) cells are increasingly recognised as contributors to allergic inflammation, yet remain less well understood than T helper 2 (Th2) cells and Group 2 innate lymphoid cells (ILC2s). Defined by production of IL-4, IL-5 and IL-13, Tc2 cells have been implicated in eosinophilic inflammation, airway hyperresponsiveness, mucus production, and chronic tissue inflammation in diseases including asthma, atopic dermatitis, and chronic rhinosinusitis. Emerging evidence suggests that Tc2 differentiation and function are shaped by alarmins, lipid mediators, hypoxia, and immunometabolic pathways involving glycolysis, fatty acid metabolism, and serotonin signalling. Compared with Th2 cells, Tc2 cells may exhibit distinct features including tissue adaptation, responsiveness to innate inflammatory cues, and relative corticosteroid resistance, suggesting non-redundant roles in sustaining chronic allergic inflammation. Current biologic therapies targeting Type 2 pathways likely influence Tc2 activity, although their effects on Tc2-driven inflammation remain unclear. Here, we review current understanding of Tc2 cell phenotype, differentiation, immunometabolic regulation, and effector functions, and summarise evidence linking Tc2 cells to allergic disease. We also highlight key unanswered questions regarding Tc2 lineage stability, tissue residency, antigen specificity, and therapeutic targeting. Together, these findings position Tc2 cells as emerging amplifiers of Type 2 immunity and potential contributors to treatment-resistant allergic disease. - Source: PubMed
de Souza Ferreira SabrinaTibbitt Christopher Andrew