TARC CCL17, Human
- Known as:
- TARC CCL17, Human
- Catalog number:
- Z02840-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- TARC CCL17 Human
Related genes to: TARC CCL17, Human
- 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 CCL17, Human
Related articles to: TARC CCL17, Human
- The IL-23/Th17 axis is the cornerstone of psoriasis pathogenesis, but molecular heterogeneity across different ethnicities remains poorly defined. - Source: PubMed
Publication date: 2026/07/02
Chen Chung-HanLee Meng-SuiChang Wen-YuCho Yung-TsuLu Yea-TingHuang Wen-LiChu Chia-YuTsai Tsen-FangKrueger James GChan Tom C - The nutritional quality of pork, a vital source of protein in the human diet, is being increasingly studied due to health concerns regarding pork fatty acid (FA) composition. Therefore, the primary objective of this study was to identify the relationship between muscle gene expression and the composition of different FAs in pigs, focusing on the two prevalent genotypes (AA and AB) from hotspot expression quantitative trait loci (eQTL) regions within the study population. This was achieved through the application of weighted gene co-expression network analyses (WGCNA) based on RNA-Seq data from 72 pigs to construct gene co-expression clusters and correlate them with the FA profile of skeletal muscle in pigs. The WGCNA was constructed using RNA-Seq data normalized to transcripts per million (TPM) across three hotspot eQTL regions: SSC3 (102,983,783 bp), SSC2 (67,926,641 bp), and SSC6 (93,742,864 bp). - Source: PubMed
Publication date: 2026/06/29
Durval Mariah CastroBrito Luiz FFanalli Simara LarissaCiconello Fernanda NeryOliveira Camila SabinoNascimento Lucas Echevarriada Silva Bruna Pereira MartinsCesar Aline Silva Mello - Myocardial infarction (MI) disrupts immune homeostasis by impairing the recruitment and suppressive function of regulatory T cells (Tregs), which are hard to restore to date. In this study, a dual-functional platform based on core-shell microgels (Ab/HAPA C-S MGs) was developed to enhance Tregs homing and function within the post-infarct environment. The surface-modified C-C motif chemokine ligand 17 (CCL17) antibody neutralized excess CCL17, thereby enabling targeted Tregs recruitment. Propionic acid (PA) was released via hydrolytic cleavage of an encapsulated prodrug precursor (HAPA) within the core to promote Tregs immunosuppressive activity through fatty acid oxidation. The platform ensured localized retention and release of PA, addressing the pharmacokinetic limitations characteristic of short-chain fatty acid (SCFAs). The Ab/HAPA@C-S MGs enhanced Tregs recruitment by 4.2-fold through CCL17 neutralization, while enzymatically released PA boosted Tregs immunosuppression with 1.8-fold higher Foxp3 expression . In MI models, treatment with Ab/HAPA@C-S MGs promoted a 2.4-fold increase in Tregs infiltration while reducing Th17 cells in infarcted region, ultimately improving cardiac functions and attenuating myocardial fibrosis. These findings show potential of the SCFA-based C-S MGs system on regulating the immunomodulation and cardiac tissue repair. - Source: PubMed
Publication date: 2026/06/16
Song LiangKang YongyuanPeng PaiWang QiaoxuanWang ShuqinShen LiyinZhang JinyueZhu YangGao Changyou - The persistent HIV reservoir constitutes the main obstacle to curing HIV/AIDS disease. Our understanding of how non-productive HIV infections are established in primary human CD4 T cells during the first round of infection is still incomplete. In this study, we leverage the HIV reporter virus pMorpheus-V5 to delineate cellular expression patterns upregulated in non-productively infected stem cell memory (T) CD4 T cells. We find that CD4 T harboring non-productive proviruses display a distinct transcriptomic signature comprising 118 upregulated genes, distinct from that of productively infected cells as well as from negative-exposed and mock-infected cells. Among the cellular genes most upregulated in CD4 T cells harboring non-productive proviruses are CCR4-binding migratory chemokines (CCL22, CCL17), tryptophan catabolic enzymes (IDO1, KYNU), and genes encoding cytoskeletal rearrangement proteins (BASP1, TNFAIP2). Flow cytometry-based analyses confirm that non-productively infected CD4 T cells are enriched for CCL22 and IDO1 co-expression compared to other CD4 T memory subsets, underscoring a CD4 T cell subset specificity for the upregulation of these two immune gene sets associated with non-productive infections. These findings suggest that primary human CD4 T harboring non-productive proviruses display a distinct immunoregulatory phenotype which may facilitate immune evasion and contribute to the persistence of the HIV reservoir. - Source: PubMed
Publication date: 2026/06/25
Butta Giacomo MAlburquerque BremyKearns CharlotteHadas YoavVanDyck Max WScaglioni SusannaPeña NoahWong Hoi TongLevendosky ElizabethGleason CharlesLin XiaoManganaro LaraPinto DalilaMulder Lubbertus C FSimon Viviana - Atopic dermatitis (AD) is a chronic inflammatory skin disorder driven by Th2-related cytokines, including interleukin-4 (IL-4) and IL-13. Recent single-cell sequencing and proteomic studies have demonstrated that sustained immune activity can persist even after treatment with the anti-IL-4 receptor alpha antibody dupilumab. Thus, targeting C-C chemokine receptor 4 (CCR4), which is highly expressed by Th2 cells and drives their migration into the inflamed tissues such as skin in response CCL17 (TARC) and CCL22 (MDC), could be a promising therapeutic approach for the treatment of AD. - Source: PubMed
Publication date: 2026/06/26
Dahabreh DantePatel DevDel Duca EsterCorriden RossBrockstedt Dirk GGuttman-Yassky Emma