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
- PIWILs are RNA-binding proteins whose role in ischemic stroke remains poorly defined. Here, we investigated the contribution of PIWILs to post-ischemic neuroinflammation by using a mouse model of 1 h transient middle cerebral artery occlusion (tMCAo), followed by 6 or 24 h of reperfusion. Brain tissues, blood, and peripheral organs were collected to assess PIWIL expression, inflammatory responses, and brain damage. PIWIL1 and PIWIL2 were significantly upregulated in the cortex and striatum at 24 h post-ischemia, with PIWIL2 also increased in blood and peripheral tissues. Immunofluorescence analyses revealed cell-type-specific localization of PIWILs in neurons, astrocytes, and endothelial cells. Notably, siRNA-mediated silencing of PIWIL2 significantly reduced infarct volume. PIWIL2 silencing also attenuated NF-κB-p65 and phospho-IκBα levels in the peri-infarct cortex but not in the striatum, indicating region-specific modulation of NF-κB signaling and differentially reprogrammed systemic chemokine profiles, with selective upregulation of CCL3, CCL5, and CXCL13 and downregulation of CCL2, CCL17, CCL20, and CXCL1. Mechanistically, PIWIL2 interacted with IKKα and promoted activation of the NF-κB pathway, leading to RelA- and RelB-dependent transcriptional regulation of pro-inflammatory chemokines. Together, these findings identify PIWIL2 as an upstream regulator of NF-κB-dependent neuroinflammation that exacerbates ischemic brain injury and suggest PIWIL2 as a promising therapeutic target targeting post-stroke inflammatory damage. - Source: PubMed
Publication date: 2026/07/24
Patil Rohan MaheshLaudati GiusyGuida NatasciaRuggiero SilviaDi Muraglia NoemiAnzilotti SerenellaLanthaler JulianCoppola LuigiFormisano LuigiAnnunziato LucioEsposito ElgaPignataro Giuseppe - Asthma is a chronic inflammatory disease affecting over 300 million people worldwide. This disease has multiple underlying etiologies, and a major endotype of asthma is characterized by cellular and molecular signatures of type 2 (allergic) inflammation. In this study we conducted bronchoscopies with airway segmental allergen challenge in allergic asthmatics to dissect airway responses to allergen. Using mass cytometry and single-cell RNA sequencing, we characterized with high resolution the airway immune landscape before and after allergen challenge and the heterogeneity present between subjects. This heterogeneity generally falls along a type 1/ type 2 axis. In type 2 high individuals, we identified allergen-reactive Th2 cells by using TCR sequences to barcode clonal T cell populations in single-cell genomic and activation-induced marker expression assays. These potentially pathogenic Th2 cell clones were present systemically and expanded following allergen challenge, connecting local lung inflammation to systemic clonal Th2 cell dynamics. Th2 cell airway ingress was coordinated with myeloid cell expression of T cell chemoattractants including CCL17 and CCL22. This study provides insight into the molecular and cellular components of allergen-induced tissue inflammation in asthma. Deeper resolution of the T cell response to aeroallergens may inform novel diagnostic and therapeutic strategies for asthma and other allergic airway diseases. - Source: PubMed
Publication date: 2026/08/06
Wheeler Benjamin DWang JingmingNerella SrilaxmiJohansson KristinaGarudadri SureshMuñoz-Sandoval PriscilaMazumder ThomasChristenson Stephanie ABhakta Nirav RErle David JAnsel K MarkWoodruff Prescott G - CSF inflammatory biomarkers in Huntington disease (HD), a neurodegenerative CAG-triplet expansion disorder, usually increase with disease progression. CSF leukocytes as an inflammatory marker have not been explored in HD. We explored high-precision CSF-leukocyte counts across different HD stages in the multicenter prospective biosample HD study HDClarity and their association with CSF neurofilament light chain (NFL) and cytokine and chemokine patterns. - Source: PubMed
Publication date: 2026/08/17
Gao YuÁsbjörnsdóttir BirnaVinther-Jensen TuaVon Essen Marina RodeHellem Marie Nathalie NickelsenHjermind Lena EEjlerskov PatrickLandwehrmeyer G BernhardSellebjerg FinnNielsen Joergen ErikLewerenz Jan - - Source: PubMed
Publication date: 2026/08/02
Zhang XinLi JiayanXu LuGuo XiaoqingEscames GermaineAcuña-Castroviejo DaríoZhao HuadongNi YunfengYang Yang - Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation, altered differentiation, barrier dysfunction, and oxidative stress. Currently available therapies, including monoclonal antibodies and JAK inhibitors, have improved AD management but do not address all aspects of the disease, supporting the investigation of natural-product strategies as complementary approaches to long-term care. An acute in vitro model of canine atopic-like inflammation was established by exposing canine progenitor epidermal keratinocytes (CPEK) for 24 h to a defined cytokine cocktail (IFN-γ, IL-4, IL-13), followed by 24 h of treatment with hemp oil, blackcurrant seed oil, vitamin D, or their combination. Proliferation (Ki-67, cell-cycle), differentiation (KRT5, KRT10, TGM1, involucrin), tight-junction organization (CLDN1, TJP1, ZO-1, TEER), wound closure, nitrosative stress (3-nitrotyrosine), the NRF2/BACH1/HMOX1 axis, and the secretion of STAT1- and NF-κB-dependent inflammatory mediators (CXCL9, CXCL10, IL-8, IL-6) and the STAT6-targeted chemokine CCL17 were assessed. The cytokine cocktail induced a coherent AD-like phenotype: increased Ki-67, downregulated CLDN1, sustained nitrosative stress, NRF2 elevation paralleled by BACH1 induction, and robust secretion of STAT1- and NF-κB-dependent mediators. The four treatments modulated this phenotype according to clearly differential, pathway-specific profiles. Vitamin D, alone or combined, emerged as the most effective modulator of proliferation and acted preferentially on the downstream redox arm, inducing HMOX1 and reducing BACH1; both vitamin D-containing formulations exerted broad anti-inflammatory activity across the STAT1 and NF-κB axes. Hemp oil acted preferentially on tight-junction integrity (CLDN1 recovery), on the upstream NRF2 arm (NFE2L2 induction), on the STAT1 chemokine arm (CXCL9, CXCL10 reduction), and on wound closure. Blackcurrant seed oil acted preferentially on NF-κB-dependent IL-8 and on early wound-closure dynamics. This differential pharmacological footprint provides a rational basis for further investigation of these formulations as nutraceutical adjuncts in canine AD. - Source: PubMed
Tortolani DanielScipioni LuciaAnselmucci AlessandroCiaramellano FrancescaDi Leonardo MeriFusaro IsaOddi SergioGramenzi Alessandro