CCL17 Antibody
- Known as:
- CCL17 Antibody
- Catalog number:
- XW-7738
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCL17 Antibody
Related genes to: CCL17 Antibody
- Gene:
- CCL17 NIH gene
- Name:
- C-C motif chemokine ligand 17
- Previous symbol:
- SCYA17
- Synonyms:
- TARC, ABCD-2
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2016-10-05
Related products to: CCL17 Antibody
Related articles to: CCL17 Antibody
- Kawasaki disease is an acute systemic vasculitis, and the clinical significance of serum thymus and activation-regulated chemokine (TARC) remains incompletely understood. We examined whether pre-treatment age-adjusted serum TARC was associated with inflammation-based intravenous immunoglobulin (IVIG) resistance risk stratification. - Source: PubMed
Tomori ShinyaTakahashi KazuhiroKoyama TakayukiMimaki Masakazu - Although most upper respiratory tract infections (URTIs) have a viral etiology, antibiotics are widely prescribed, thus contributing substantially to antimicrobial resistance. This study investigated the potential beneficial effects of a novel strain, LMG P-27481, against major URT pathobionts (, , , , and ) with the aim of reducing or delaying antibiotic use. Antibacterial and immunomodulatory activities were evaluated using alone or combined with resveratrol, a natural compound with antiviral and anti-inflammatory properties. Both agents inhibited pathogen growth, while their combination showed additive antibacterial activity, particularly against Gram-negative bacteria. Antioxidant assays demonstrated significant antioxidant capacity for both agents, with enhanced effects in combination in NBT and ABTS assays but antagonistic in ORAC. Immune mediators (IL-6, IL-8, IL-1β, TNF-α, IL-25, IL-33, CCL17, CCL22) were assessed in epidermal, epithelial, and macrophage cell lines, together with epidermal integrity markers (Filaggrin, Loricrin, Involucrin) in a 3D reconstructed human skin model (EpiDermFT). , resveratrol, and their combination exerted cell-specific effects in the different models, modulating cytokine expression and production, and barrier integrity. Our findings support the potential efficacy of oral LMG P-27481 plus resveratrol in URTIs. - Source: PubMed
Publication date: 2026/08/12
Mattioli RobertoDi Risola DanielSivori FrancescaFranzese OrnellaGenovese IlariaMastromarino PaolaMosca Luciana - : Atopic dermatitis (AD) is a persistent and recurring skin disease characterized by epidermal barrier dysfunction, immune dysregulation, and elevated expression of proinflammatory mediators. We investigated the anti-inflammatory potential of polynucleotides (PN), highly purified DNA biopolymers isolated from salmonid gonads, in keratinocyte and macrophage activation models. : RAW 264.7 macrophages were stimulated with lipopolysaccharide (LPS), whereas HaCaT keratinocytes were stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The effects of PN treatment on the production or expression of inflammatory mediators, cytokines, and chemokines were evaluated. Changes in the phosphorylation of mitogen-activated protein kinases (MAPKs) and Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) and in the nuclear localization of nuclear factor-κB (NF-κB) were also assessed. : In LPS-activated RAW 264.7 macrophages, PN treatment significantly suppressed nitric oxide production and downregulated the expression of inducible nitric oxide synthase (iNOS), TNF-α, IL-1β, and IL-8, accompanied by reduced NF-κB nuclear translocation. In TNF-α/IFN-γ-stimulated HaCaT keratinocytes, PN treatment markedly decreased the secretion levels of IL-6, IL-1β, and thymic stromal lymphopoietin. Moreover, PN treatment markedly reduced T-cell-recruiting chemokines, including MDC/CCL22, TARC/CCL17, RANTES/CCL5, and IL-8. Signaling analyses demonstrated that PN treatment attenuated the phosphorylation of key MAPKs (ERK, JNK, and p38) and the JAK1/STAT3 axis. Furthermore, PN treatment markedly reduced NF-κB nuclear translocation. : These in vitro findings indicate that the anti-inflammatory effects of PN are associated with reduced activation of multiple core signaling pathways governing cytokine and chemokine responses, supporting further investigation of PN in AD and other chronic inflammatory skin diseases. - Source: PubMed
Publication date: 2026/08/13
Ha Ye JinTak Ka HeeLee Jong LyulKim Chan WookMoon Ik JunYoon Yong Sik - The inflammatory response is central to the pathogenesis of alcohol-associated liver disease (ALD), yet currently used prognostic scores, including Maddrey's modified discriminant function (mDF), Child-Turcotte-Pugh (CTP), MELD-Na and MELD 3.0, reflect hepatic synthetic and excretory function rather than the underlying immune alterations. Since CC-motif chemokines (CCLs) regulate immune cell trafficking and hepatic stellate cell activation, they warrant deeper investigation, as reports on their role in ALD remain limited. Therefore, the primary objective of this study was to evaluate the diagnostic and prognostic performance of selected serum CCLs, and to correlate their levels with disease severity and short-term survival in patients with ALD. Serum MIP-3α/CCL20, MCP-1/CCL2 and TARC/CCL17 were measured in 63 patients with ALD and 25 healthy controls using ELISAs. Chemokine concentrations were correlated with liver function tests, inflammatory indices and short-term (30-day) survival. The diagnostic and prognostic performances of individual CC chemokines were assessed by ROC analysis and by univariate and multivariable logistic regression. MIP-3α/CCL20 was increased more than 11-fold in ALD versus healthy controls and reached an AUC of 0.978 for distinguishing the two groups in a case-control comparison (a proof-of-principle, case-control result which requires validation against other chronic liver diseases). It increased across Child-Turcotte-Pugh classes and correlated with all other prognostic scales. MCP-1/CCL2 was significantly elevated in the ALD group but did not discriminate ALD severity. TARC/CCL17 was significantly lower in ALD than in controls. On multivariable regression, MIP-3α/CCL20 was the dominant predictor of both ALD status and severe liver dysfunction. In patients with ALD, MIP-3α/CCL20 appears to bridge hepatic inflammation and hepatocellular failure and is a candidate exploratory biomarker of disease severity that requires further confirmation against other chronic liver diseases. The short-term mortality analysis was based on only seven events. This evaluation is exploratory and underpowered, and its findings should not be interpreted as definitive prognostic evidence. MCP-1/CCL2 does not stratify ALD severity. Decreased TARC/CCL17 concentrations point to a separate immunoregulatory failure and are presented as a hypothesis requiring mechanistic testing in pre-clinical models. - Source: PubMed
Publication date: 2026/08/10
Szczerbinska AgnieszkaRolinski JacekSurdacka AgataCichoz-Lach Halina - Nucleated erythroid cells (NECs) are emerging as important immunoregulators at the feto-maternal interface, yet their chemokine profiles and functional dynamics across pregnancy remain poorly understood. Using a murine allogeneic pregnancy model (CBA × C57Bl/6), we isolated placental and splenic TER-119 NECs at mid- (E12.5) and late (E19.5) gestation. Chemokine production (13-plex), chemokine receptor expression (qPCR), immunosuppressive molecules (PD-L1, TGF-β, and ROS), T-cell proliferation (CFSE), and immune cell migration (Transwell) were assessed. CD45 placental NECs were the main producers of PD-L1, TGF-β, and ROS, with maximal expression at E19.5, suggesting their potential contribution to the immunosuppressive functions observed in the total TER-119 population. Chemokine production showed a striking shift in CCL17 and CXCL9 from the spleen to the placenta as pregnancy advanced (E12.5 → E19.5). Splenic NECs displayed dominant expressions of CCR3 and CXCR4. Unexpectedly, CCL2 and CCL4 blockade enhanced immune cell migration toward placental NECs at E19.5. Placental nucleated erythroid cells potently suppressed T-cell proliferation at E12.5, and this suppressive capacity remained stable until full term. Placental NECs undergo dynamic chemokine reprogramming while maintaining stable T-cell suppression. The paradoxical enhancement of migration after CCL2/CCL4 blockade suggests a complex chemokine network warranting further investigation. These findings provide new insights into the immunobiology of pregnancy and may have implications for understanding pregnancy complications. - Source: PubMed
Publication date: 2026/08/08
Shevchenko Julia ANazarov Kirill VGizbrekht Alina ASavostyanova Tatyana AZakhareva Alena PSennikov Sergey V