Mouse CXCL10 ELISA Kit
- Known as:
- Mouse CXCL10 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1745
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Mouse CXCL10 ELISA Kit
Related genes to: Mouse CXCL10 ELISA Kit
- Gene:
- CXCL10 NIH gene
- Name:
- C-X-C motif chemokine ligand 10
- Previous symbol:
- INP10, SCYB10
- Synonyms:
- IFI10, IP-10, crg-2, mob-1, C7, gIP-10
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2016-10-05
Related products to: Mouse CXCL10 ELISA Kit
Related articles to: Mouse CXCL10 ELISA Kit
- Early identification of refractory disease remains a significant unmet clinical need in patients with diffuse large B-cell lymphoma (DLBCL). This scoping review was conducted to assess the current knowledge on the use of circulating tumor DNA (ctDNA), either alone or in combination with immune markers, as predictive tools for treatment outcome in previously untreated DLBCL patients. A systematic search of online databases PubMed, Embase, CINAHL, and Cochrane was performed from inception to May 2025. This focused on primary research studies investigating the use of ctDNA or immune markers to assess treatment response and predict outcomes in DLBCL. 61 publications were selected for inclusion. The key points of interest for this scoping review were: pre-analytical sample handling, laboratory methodologies-including sequencing panels and platforms; and mutations or immune markers associated with prognosis or patient outcome. Strong evidence supports the utility of ctDNA analysis at key timepoints to evaluate treatment response: diagnosis, cycle 2 day 1, cycle 3 day 1, and end of treatment. ctDNA assays with adequate sensitivity can improve interpretation of FDG-PET/CT scans, reducing unnecessary additional testing for patients. Molecular clustering on ctDNA also improves risk stratification. Elevated cytokines such as CXCL10 and IL-10 and elevated numbers of myeloid derived suppressor cells in pre-treatment samples are associated with inferior prognosis. ctDNA analysis shows promise in improving outcomes for patients with DLBCL. Assay standardization for ctDNA analysis is currently lacking. Further investigation into the additional value of immune marker analysis is required. This includes understanding the association between immune markers and molecular subgroups identified on ctDNA analysis. - Source: PubMed
McMahon AilinRyan Elizabeth JDillon SarahClifford Ruth - Diagnosing bacterial infections in children with fever without source remains challenging. The MeMed BV score, combining C-reactive protein, interferon gamma-induced protein-10, and tumor necrosis factor-related apoptosis-inducing ligand, has shown high performance in detecting bacterial infections, mostly in adults. The objective of this study is to explore the diagnostic performance of the MeMed BV score in identifying bacterial infections in young children with fever without source. In this prospective exploratory observational study, children younger than 3 years presenting to the pediatric emergency departments with acute fever without source were eligible for inclusion. An adjudication committee reviewed clinical and microbiological data to establish the diagnosis of bacterial infection. The MeMed BV score ranged from 0 to 100, with manufacturer-validated thresholds: < 35 viral, > 65 bacterial, 35-65 equivocal. In the main analysis, equivocal scores were considered bacterial. A sensitivity analysis was subsequently performed excluding patients with equivocal scores. The performance of MeMed BV score was compared to procalcitonin. Among the 384 eligible children, 69 were analyzed. Median age was 2 months (IQR 1-10), and 25% had a bacterial infection. The sensitivity of MeMed BV was 47.1% (95% CI 23.0-72.2), the specificity was 84.6% (95% CI 72.1-93.1), and the area under the curve was 0.80 (95% CI 0.69-0.92). Procalcitonin's sensitivity was 82.4% (95% CI 56.6-96.2). - Source: PubMed
Publication date: 2026/08/20
Brel AnneGras-Le Guen ChristèleLaunay EliseVrignaud BénédicteMartin Perceval LiseLorton FleurMalorey David - Banff acute lesion scores underpin histologic classification of kidney allograft biopsies; however, biomarker studies rely on second-order associations with diagnostic categories that introduce confounding. We quantified the first-order relationships between Banff acute lesion scores and the validated urinary cell three-gene rejection signature. In 354 biopsy-urine pairs, three-gene signature scores computed using a locked regression equation incorporating absolute copy numbers of CD3E mRNA, CXCL10 mRNA, and 18S rRNA in urinary cell RNA-were related to glomerulitis ( ), peritubular capillaritis ( ), interstitial inflammation ( ), and tubulitis ( ). Signature scores rose monotonically with Banff acute lesion severity, with 1.5 to 1.8-fold higher odds of more severed and (all P<0.0001), and showed good calibration. Associations remained robust for composite microvascular ( ) and tubulointerstitial ( ) indices and were strongest for severe and , supporting this signature as a noninvasive, quantitative readout of acute rejection pathology with immediate diagnostic applicability. - Source: PubMed
Publication date: 2026/07/27
Li CarolSchwartz Joseph ESalinas ThaliaDadhania Darshana MDeVito AlexHiggins WilliamSalvatore StevenSeshan Surya VSharma Vijay KMuthukumar ThangamaniSuthanthiran Manikkam - Newcastle disease virus (NDV), a significant avian paramyxovirus, depends on the acquisition of host-derived membranes for viral envelope assembly during budding. However, the relationship between NDV budding efficiency and host metabolic reprogramming remains incompletely understood. Our previous research demonstrated that the highly virulent strain Herts/33 and the non-virulent strain LaSota differ significantly in budding efficiency, which is attributed to the difference in ubiquitination levels at the K247 site of the M protein. In this study, using recombinant viruses generated in our previous study, we investigated the effects of the K247 ubiquitination site on host cell metabolism. Through RNA sequencing and LC-MS/MS, systematically profiled the transcriptional and metabolic alterations induced by these viruses in HeLa cells. We also compared organ pathology in three-week-old SPF chicks infected with Herts/33 versus LaSota. The results showed that NDV infection broadly reprograms host sphingolipid metabolism. Compared with rLaSota-WT, rLaSota-R247K exhibited higher budding efficiency, linked to accelerated ceramide depletion and a stronger innate immune response. Specifically, rLaSota-R247K infection upregulated interferon- and interleukin-related components such as ISG15, CXCL8, TNF-α, CXCL10, NOD2, CD274, OAS, and IFNB1. Furthermore, we confirmed that blocking the ceramide synthesis pathway significantly suppresses NDV-M protein-mediated budding of VLPs and virions. Pathologically, Herts/33 induced more severe tissue damage than LaSota. Together, these findings indicate that the K247 residue of the NDV M protein enhances viral budding and promotes rapid utilization of host sphingolipids. This work provides mechanistic insight into NDV budding and highlights virus-host metabolic interactions that may inform future antiviral strategies. - Source: PubMed
Publication date: 2026/08/03
Dai JunLiu FanxinFeng YiyiYou QinqinWang JiaojiaoDing ChanQiu XushengXiao Shiji - Psoriasis is a highly prevalent inflammatory skin disease for which good systemic therapeutic agents are available. However, there still is a great need for new treatment options, especially oral ones. Salt-inducible kinases (SIKs) are emerging as new druggable targets in immune diseases and the SIK2/SIK3 inhibitor GLPG3970 recently proved to efficiently reduce psoriasis lesions in a phase Ib trial. This study assesses molecular events underlying beneficial effects of SIK2/SIK3 inhibition via GLPG3970 in psoriasis. Using spatial transcriptomics and single cell sequencing, abundant expression of SIK2 and SIK3, but not of SIK1, was observed in psoriatic skin. In vitro, GLPG3970 reduced psoriasis marker cytokines and chemokines (TNF, IFN-γ, IL-1β, IL-6, CXCL8, CXCL10) in peripheral mononuclear cells, T cells and fibroblasts, but not in keratinocytes. Bulk RNA sequencing of lesional psoriasis biopsies treated ex vivo with GLPG3970 and of biopsies received from responders vs. placebo-treated patients of the clinical trial showed downregulation of inflammatory pathways with suppression of IL1B, CXCL1, CXCL8, CEBPB, CD177, and CLEC5A in both settings. In summary, this study suggests that specific inhibition of SIK2/SIK3 reduces acute phase immunity and neutrophil recruitment in psoriasis. - Source: PubMed
Publication date: 2026/08/18
Pilz Anna CarolineBriem EvaColli MaikelHillig ChristinaLavazais StephanieMenden Michael PBiedermann TiloLauffer FelixEyerich KilianDe Vos SteveJargosch Manja