Human TARC (CCL17)
- Known as:
- Human TARC (CCL17)
- Catalog number:
- GEM-300-201P20
- Product Quantity:
- 20 ug
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Human TARC (CCL17)
Related genes to: Human TARC (CCL17)
- 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: Human TARC (CCL17)
Related articles to: Human TARC (CCL17)
- Pressure ulcer (PU) typically arises as a chronic cutaneous ulcer stemming from a complex interplay of factors. However, the underlying mechanisms of this condition remain unclear. The aim of this study was to identify inflammatory biomarkers in patients with PU. In this study, PU and normal tissues were collected from 24 patients with PU. An exploratory Olink Inflammation Panel analysis was performed to identify candidate differentially expressed proteins (DEPs) between PU and normal tissue samples from 16 of the 24 patients with PU. A total of 16 candidate DEPs were identified using an unadjusted p < 0.05 threshold between the two groups. Among them, CCL17 had the largest fold change and diagnostic potential with an optimal AUC value (0.75). In addition, CCL17, ANGPT1, FASLG, and VEGFA demonstrated high clinical relevance in the patients with PU. Immunohistochemistry and western blotting using PU tissues obtained from the remaining 8 patients confirmed the decreased expression of CCL17 in PU tissues. In conclusion, CCL17 is a novel potential biomarker for PU pathogenesis and prognosis. - Source: PubMed
Publication date: 2026/09/20
Wu LinjunZhou ShihanLi ShiqinChen YangLuo YingZhang DanCai XuchaoWang ChenmingFan LeiZhu MingliZeng LonghuanZheng Yongke - Kidney transplant recipients are subjected to several types of immunosuppressants in order to prevent rejection of the graft. Over-immunosuppression increases the risk of infectious complications and thesepatients require a delicate balance. Inflammatory profiles from the urine can help identify which biomarkersmay guide clinicians in balancing over vs. under-immunosuppression. - Source: PubMed
Publication date: 2026/08/31
Spiwak ElizabethNailescu CorinaHains David SKolner MarahArregui SamualSchwaderer Andrew L - Primary mediastinal large B-cell lymphoma (PMBCL) predominantly affects female adolescents and young adults. It displays an immune-privileged phenotype and demonstrates the involvement of key cytokine signaling pathways, including increased expression of Thymus and activation-regulated chemokine (TARC/CCL17). Currently, there is a lack of established markers for stratification. We studied plasma concentrations of 24 cytokines at diagnosis in a large population-based pediatric cohort of 62 patients with PMBCL. Compared to a group of age-matched patients with other types of lymphoma in long-term remission and healthy individuals (n=26), we detected elevated concentrations of CCL4, CCL17, interleukin (IL)-6, CXCL8, CXCL9, CXCL10, and CXCL11. The median CCL17 level was 1695 pg/ml (IQR, 642-3142) in patients with PMBCL compared to 81 pg/ml (IQR, 41-190) in controls (p < 0.0001). Concentrations of CCL17, CXCL9, and CXCL10 significantly correlated with mediastinal tumor volume (MTV) and lactate dehydrogenase activity (LDH) but were not associated with event-free survival (EFS). Concentrations of IL-17F and IL-22 were inversely correlated with LDH and MTV. Elevated IL-6, IL-10, IL-17A, and IL-22 were significantly correlated with inferior EFS in a subgroup of 50 patients uniformly treated with dose-adjusted EPOCH with rituximab. Although based on a limited number of events, IL-6 showed the strongest association with outcome (hazard ratio of 6.8 (95%-CI, 1.5-30.9). In summary, pretreatment cytokine levels in patients with PMBCL reveal distinct patterns associated with tumor burden (CCL17, CXCL9, CXCL10) and outcome (IL-6, IL-10, IL-17A, IL-22). - Source: PubMed
Publication date: 2026/09/10
Nipper MalteDamm-Welk ChristineShepheard WillOschlies IlskeKlapper WolframBurkhardt BirgitWoessmann WilhelmKnörr Fabian - Tet2 dysfunction drives myeloid neoplasm initiation and progression, yet the mechanisms underlying disease heterogeneity, age-dependent progression and immune microenvironment perturbation remain poorly understood. This study aimed to establish a hematopoietic specific Tet2 conditional knockout mouse model to elucidate these core mechanisms and recapitulate clinical features of Tet2 mutated myeloid neoplasms. - Source: PubMed
Publication date: 2026/09/08
Chen YanxiYu LiYang RuiChen PengjieZeng WenLi ZihanWang YantingXu YonggangYang Xiupeng - T cells are often enriched at barrier tissues, yet little is known of their roles in barrier sensing and relevance to associated disease. CD1a is a Major Histocompatibility Complex class I-like molecule expressed by Langerhans cells, which forms complexes with lipid antigens to facilitate recognition by non-classical CD1a-reactive T cells. - Source: PubMed
Publication date: 2026/09/08
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