CCL21 Antibody
- Known as:
- CCL21 Antibody
- Catalog number:
- XW-7739
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCL21 Antibody
Related genes to: CCL21 Antibody
- Gene:
- CCL21 NIH gene
- Name:
- C-C motif chemokine ligand 21
- Previous symbol:
- SCYA21
- Synonyms:
- SLC, exodus-2, TCA4, CKb9, 6Ckine, ECL
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2016-10-05
Related products to: CCL21 Antibody
Related articles to: CCL21 Antibody
- The transcription factor Runx3 modulates key gene expression programs important for the development of multiple tissues. Here, we uncover new functions for Runx3 in thymic epithelial lineage development and show Runx3 expression in medullary thymic epithelial cells (mTECs) is required for both Autoimmune Regulator + (Aire) mTEC development and tissue-specific antigen (TSA) gene expression. Consequently, TEC-specific deletion of Runx3 in mice results in a profound decrease in Aire mTECs, a global loss of TSA gene expression, and the development of autoimmunity. Moreover, loss of Runx3 in TECs results in an expansion of immature CCL21 mTECs and a loss of Aire-dependent mimetic cells. Single-cell analysis reveals Runx3 modulates core transcriptional programs in TECs that correlate with the observed cellular changes. Our findings highlight a previously undescribed role for Runx3 in mTEC development and thymic central tolerance. - Source: PubMed
Publication date: 2026/05/15
Sin Jun HyungPhillips Sloan HParent Audrey VWaterfield Michael R - Despite advances in therapies targeting hemodynamic and neurohormonal axes in heart failure (HF), incomplete reverse remodeling (RR) characterized by persistent myocardial edema and fibrosis remains a major clinical challenge. This review posits that dysfunction of the cardiac lymphatic system, a critical but understudied pathway for interstitial fluid and immune cell clearance, constitutes a fundamental barrier to complete myocardial recovery. We synthesize current evidence outlining the anatomy, developmental biology, and physiological role of cardiac lymphatics in maintaining myocardial fluid homeostasis and immune surveillance. In the context of HF, the lymphatic system undergoes a dynamic evolution: an initial compensatory lymphangiogenic response in the acute phase facilitates the clearance of edema and inflammatory cells, while its subsequent exhaustion or impairment in chronic HF perpetuates a vicious cycle of inflammation, fibrosis, and adverse remodeling. Central molecular pathways, including the VEGF-C/VEGFR-3 axis and transcriptional regulators like PROX1/FOXC2, govern lymphatic growth, integrity, and function. Furthermore, lymphatics actively modulate post-injury immune responses via specialized mechanisms such as CCL21/CCR7-guided cell trafficking. Therapeutically, augmenting cardiac lymphangiogenesis presents a promising strategy to enhance fluid drainage, resolve maladaptive inflammation, and directly support cardiomyocyte survival, thereby creating a conducive milieu for RR. However, translating this potential requires overcoming translational hurdles related to intervention timing, comorbidity-specific lymphatic dysfunction, and the development of targeted delivery systems. This review concludes that harnessing the cardiac lymphatic system represents a paradigm-shifting therapeutic avenue, complementary to existing regimens, with the potential to promote more complete and sustainable reverse remodeling in heart failure. - Source: PubMed
Publication date: 2026/04/22
Huang TingxuanQi TengYao LingjunZhu ZhentaoLi ChenyuTang PengxiangMeng ZeyuWen ZheyuWang TingyuLiu SuiXie PeilinLi ZilinHu Jing - CC chemokine receptor 7 (CCR7), which orchestrates adaptive immunity, exhibits a phenomenon known as biased agonism. CCL19 induces robust G-protein signaling and β-arrestin recruitment, leading to transient signaling. In contrast, CCL21 preferentially activates G-protein pathways with minimal arrestin engagement, resulting in sustained signaling and differential functional outcomes. Here, we present the cryo-EM structures of the human CCR7-G complex with either CCL19 or CCL21. The structures reveal that while both engage a conserved orthosteric pocket, they adopt markedly distinct binding poses. Notably, the compact 30s loop of CCL21 inserts deeply into the receptor's extracellular vestibule, whereas the corresponding loop of CCL19 rests atop extracellular loop 2. Molecular dynamics simulations further reveal that these distinct binding modes induce differential intracellular dynamics, linked to the rotameric state of Y83 at the intracellular end of transmembrane helix 1. We demonstrate that CCL19 stabilizes a flexible conformational ensemble with a highly dynamic helix 8, creating a lateral opening favorable for GPCR kinase engagement. Conversely, CCL21 restricts this flexibility, locking the receptor in a state that precludes kinase interaction while maintaining G-protein coupling. Corroborated by functional data, these findings provide key insights into the structural basis of biased agonism at CCR7 and establish a foundation for rational design of pathway-selective immunomodulators. - Source: PubMed
Publication date: 2026/04/29
Tanaka KotaroNishikawa KoukiShiimura YukiFujiyoshi YoshinoriTsutsumi Naotaka - Primary sclerosing cholangitis (PSC) is a chronic, idiopathic cholestatic liver disease characterized by inflammation and fibrosis of the bile ducts, yet the cellular crosstalk driving periductal fibrosis remains poorly defined. This study applied a multi-omics approach integrating spatial transcriptomics, RNA-seq, and proteomics to characterize fibrotic periductal regions and their cell-cell communications. Macrophages (MP) subsets, including monocyte-drived-(Mo)MP and lipid-associated-macrophage (LAM)-like, co-localized with cholangiocytes, lymphocytes, and hepatic stellate cells (HSC1). Cell niche analysis identified periductal regions with elevated fibrotic signals, where cell-cell communication analysis revealed potential MP-HSC interactions involving 17 fibrotic driver genes in MP, including ITGB2, GRN, and CCL21, and 6 fibrotic effector genes in HSC. In validation analyses, bulk RNA-seq data showed higher driver and effector gene expression in PSC with established fibrosis compared to early-stage PSC or healthy control (HC). Plasma proteins encoded by MP driver genes were elevated in PSC and in patients with elevated (≥3.29 kPa) liver stiffness on MR elastography. Furthermore, immunofluorescence and SHG imaging showed enrichment of CD68+/CD18+(ITGB2) macrophages in fibrotic regions of PSC liver biopsies. These findings revealed enrichment of MoMP and LAM-like macrophages in fibrotic regions and suggest that they likely contribute to fibrotic activation of nearby HSCs in PSC. - Source: PubMed
Publication date: 2026/04/23
Wang YunguanAdeleke DavidXie XiangfeiYang Zi FWang XiangyaLoi GiuliaYang Vom Hofe AnnikaSingh ManaviMalik AsthaKudira RameshCastro-Rojas CydPfuhler LivaAlquraish MosabSylvestre PamelaDillman Jonathan RTrout Andrew TMiraldi Emily RMiethke Alexander G - Samples often have to be frozen and thawed prior to analysis for immunoassays. Reliable cytokine measurement from small-volume plasma and serum samples is critical for biomarker research and clinical studies. However, repeated freeze-thaw (F-T) cycles may alter analyte stability, introducing error and reducing reproducibility. Standard statistical methods often overlook donor-to-donor and matrix variability, leading to overestimation of F-T effects. We measured 80 cytokines across three donors, three matrices (EDTA-plasma (PL-EDTA), heparin-plasms (PL-heparin), serum), and four F-T cycles using an 80-plex Luminex immunoassay. Linear mixed-effects modeling was applied to partition donor, matrix, and F-T contributions, while principal component analysis (PCA) summarized global variance. Cytokines were classified as stable, decreasing, or matrix-specific based on within-matrix slopes and matrix×cycle interactions. Stability was defined as the absence of a statistically significant per-cycle change (p ≥ 0.05) within all matrices, corresponding to changes smaller than typical assay imprecision (CV%). PCA revealed that donor and matrix were the dominant sources of global variation, whereas F-T cycles contributed minimally. Most cytokines remained stable (no significant within-matrix slope across cycles; p ≥ 0.05 in all matrices) across four cycles, with only a minority showing monotonic decreases. Matrix context strongly influenced F-T effects: PL-heparin displayed both increases and decreases, PL-EDTA was largely stable, and serum showed decreases without increases. Representative analytes highlighted the three categories: IL17E/IL25 and IL27 decreased modestly across matrices, chemokines such as 6CKINE/CCL21 remained stable, and analytes like SDF1A + B/CXCL12 showed matrix-specific increases. Freeze-thaw cycling contributes far less to cytokine variability than donor or matrix effects. Most cytokines are robust across four cycles, and when F-T sensitivity occurs, it is largely matrix-dependent. These results provide evidence-based guidance for sample handling and highlight the importance of modeling donor and matrix effects in biomarker studies. - Source: PubMed
Publication date: 2026/04/08
Verma ArushiSridharan KeshavHerschmann IrisNguyen TranMaecker Holden T