Ask about this productRelated genes to: TARC 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: TARC antibody
Related articles to: TARC antibody
- Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease with known ethnic disparities in clinical presentation and treatment response. However, molecular data, particularly for Hispanic patients, remain limited. - Source: PubMed
Publication date: 2026/04/25
Liu DanielDel Duca EsterBrunner PatrickAvallone GianlucaBeaziz JessicaMetukuru RagasrutiLin XinyiEstrada YerielLau MeganLargen JosephUngar BenjaminGuttman-Yassky Emma - High-frequency pulsed electromagnetic fields (HF-EMF) are increasingly encountered in modern environments, yet their potential immunomodulatory effects remain unclear. Here, we investigated whether L-band pulsed HF-EMF modulate cytokine responses in human THP-1 monocytes under basal conditions or during lipopolysaccharide (LPS)-induced inflammation. Cells were exposed to pulsed electric fields at 4.6 or 7.3 kV/m, with two exposure regimens applied at each intensity (intermittent 30 s bursts or continuous 1 h exposure). Cell viability, morphology and lipid peroxidation (MDA) were assessed, and cytokine secretion was profiled by cytokine array and multiplex immunoassay, complemented by PCA and correlation network analyses. HF-EMF exposure did not induce cytotoxicity or marked oxidative damage. Under LPS stimulation, HF-EMF produced subtle yet consistent shifts in cytokine patterns, with trends toward attenuation of LPS-elevated mediators including VEGF, IL-6 and CCL17/TARC at higher field intensity. In unstimulated cells, cytokine levels remained largely unchanged, except for a reproducible decrease in basal VEGF under the highest exposure condition. Overall, these data support a context-dependent immunomodulatory effect of pulsed HF-EMF in human monocytes, warranting follow-up studies in more physiological models and with refined exposure characterization. - Source: PubMed
Publication date: 2026/04/23
Dekali SamirJolly NicolasDe Araujo SuzanneBallestra FranckJaoui RachidHermann Eve-HortenseValente MarcoDel Vecchio Flavia - Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - Mycosis fungoides (MF) is a disease that evolves slowly over years with few options for curative treatment. Improving health-related quality of life (HRQoL) is therefore an important treatment goal. This study aims to contribute to a better understanding of HRQoL, using a dermatology-adapted HRQoL questionnaire, Dermatology Life Quality Index (DLQI), in patients with MF. Baseline data from a cohort study (BIO-MUSE) of patients with MF wasere used to investigate which aspect of DLQI is the most affected and how DLQI relates to different clinical and physiological parameters. Data from a period of 12 months were used to study how DLQI changes over time. The symptom domain, for example itching, was the aspect of the DLQI that had the greatest impact on HRQoL. Thymus and activation-regulated chemokine (TARC)/ chemokine (C-C) ligand 17 (CCL17) were analysed in blood and were shown to have a positive correlation with DLQI (r=0.482, p=0.043). It was further shown that increased itching at baseline was a strong predictor of a worse DLQI score in the domain of symptoms (r=0.677, p=0.002). Future research in a larger cohort is needed to investigate the effect of itch in HRQoLhealth-related quality of life in patients with MF. - Source: PubMed
Publication date: 2026/04/22
Hub DariaDrott KristinaBelfrage EmmaSonesson Andreas - Chemokine (CC motif) ligand 17 (CCL17), an inflammatory chemokine, has been shown to mediate pain and inflammation in animal models of arthritis. However, the specific molecular mechanisms by which CCL17 mediates its inflammatory functions remain largely unknown. Matrix metalloproteinases (MMPs), particularly MMP9 and MMP13, are cartilage degrading enzymes that are known to contribute to joint pain and inflammation in arthritis. These MMPs, produced in significant quantities by macrophages, facilitate the breakdown of the extracellular matrix and are regulated by various signaling pathways, including extracellular signal-related kinase (ERK1/2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). However, how CCL17 regulates downstream mediators in arthritis has not yet been elucidated. This study investigates the regulatory role of CCL17 on MMP expression in peripheral blood mononuclear cells (PBMCs) and plasma from rheumatoid arthritis (RA) patients, as well as in monocyte-derived macrophages (MDMs) from healthy donors. Analysis of RA patient samples revealed a positive correlation between CCL17 levels and MMP9/MMP13 expression. Furthermore, CCL17 treatment of MDMs resulted in an upregulation of MMP9 and MMP13 expression, correlating with increased activity of ERK1/2 and NF-κB. Markedly, pre-treatment with pharmacological inhibitors, U0126 (an ERK1/2 inhibitor) and NF-κB Activation Inhibitor IV (NF-κB inhibitor), in both MDMs and RA PBMCs, demonstrated that CCL17-driven MMP9 and MMP13 expression was critically dependent on ERK1/2 and NF-κB activation. Our findings provide new insights into possible mechanisms driving joint destruction in RA, highlighting potential benefits of targeting CCL17 and/or its downstream mediators as potential therapeutic strategies for treating inflammation. - Source: PubMed
Publication date: 2026/04/20
Balendran ThivyaHourani TetianaGaneshalingam SubothiniHatch KatherineFletcher SamuelHor CecilLee Kevin M CHamilton John ALim KeithAchuthan Adrian A