CCR8 (Extracellular Loop) Peptide
- Known as:
- CCR8 (Extracellular Loop) Peptide
- Catalog number:
- 2097P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CCR8 (Extracellular Loop) Peptide
Related genes to: CCR8 (Extracellular Loop) Peptide
- Gene:
- CCR8 NIH gene
- Name:
- C-C motif chemokine receptor 8
- Previous symbol:
- CMKBRL2, CMKBR8
- Synonyms:
- CY6, TER1, CKR-L1, GPR-CY6, CDw198
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-10-05
Related products to: CCR8 (Extracellular Loop) Peptide
Related articles to: CCR8 (Extracellular Loop) Peptide
- Tissue resident memory (TRM) cells are of interest in chronic inflammatory skin diseases as they are believed to facilitate flares in the same anatomical area. IL-15 is an essential growth factor for the survival of TRM in the skin compartment. A main source of IL-15 are tissue-resident cells. - Source: PubMed
Publication date: 2026/04/25
Alase Adewonuola AMann CarolineKolb AntoniaWagle Sakshi VasantKlein MatthiasKramer DanielaWittmann Miriam - Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) are the primary histological subtypes of cervical cancer. Although the AGPAT family of enzymes is implicated in various cancer types, the specific roles of its members in cervical cancer remain unclear. In the present study, we investigated the value of AGPAT1-5 as potential biomarkers and therapeutic targets in cervical cancer by assessing their impact on disease development and outcomes. AGPAT gene expression data and clinical information from 306 patients with CESC and three control subjects were collected from The Cancer Genome Atlas. Given the limited number of normal cervical samples in TCGA (n = 3), we utilized the GEPIA database to integrate GTEx normal cervical samples (n = 10) as controls for differential expression analysis. These data were analyzed for differential gene expression, gene-gene and protein-protein interactions, prognostic and diagnostic value, clinical correlations, functional enrichment, and various tumor-infiltrating immune cell types. Validation was performed using two independent Gene Expression Omnibus (GEO) datasets (GSE6791 and GSE63514). The study revealed that AGPAT4 mRNA expression was significantly downregulated in cervical cancer tissues compared to normal tissues in the GEPIA analysis, while AGPAT1, AGPAT2, AGPAT3, and AGPAT5 showed no significant differences. Validation in GEO datasets demonstrated that AGPAT1, AGPAT2, and AGPAT3 were consistently downregulated in tumor tissues, whereas AGPAT5 was upregulated, and AGPAT4 showed no significant change. High levels of AGPAT3 and AGPAT4 expression, in particular, were associated with a worse prognosis in CESC patients. Immune infiltration analysis restricted to CESC samples revealed that AGPAT3 expression was significantly correlated with multiple immune cell types, including positive correlations with Macrophages M1, T cells CD4 memory resting, and Monocytes. Furthermore, guided by functional enrichment analysis implicating immune-related pathways, we examined the correlation between AGPAT3 expression and key T cell regulatory molecules, including FOXP3, IL2RA, IKZF2, and CCR8, revealing significant positive associations. In vitro assays demonstrated that knocking out AGPAT3 expression significantly decreased the proliferation and migration of HeLa and C-33 A cervical cancer cell line. These results suggest that AGPAT3 could be a valuable biomarker and a promising therapeutic target in cervical cancer. - Source: PubMed
Publication date: 2026/06/09
Gui NannanPan HanyiLu WeijuanPan GuiqiongZhou XiaoyuChen YuzhenJin MingyangYang ChangyongDong MingyouLiang Yuexiu - Inferring cellular dynamics from static single-cell data remains a central challenge in genomics. We introduce ArchVelo, a computational framework for modeling gene regulation and inferring trajectories from paired single-cell chromatin accessibility (scATAC-seq) and transcriptomic (scRNA-seq) data. ArchVelo represents chromatin accessibility as archetypes-shared regulatory programs-to model their dynamic influence on transcription. It outperforms existing methods in trajectory inference accuracy and gene-level latent time alignment, enables trajectory decomposition into archetypal components, and identifies the underlying transcription factors. After benchmarking on mouse brain and human hematopoiesis datasets, we apply ArchVelo to CD8 T cells in viral infection and reveal distinct trajectories of differentiation and proliferation. Focusing on progenitor exhausted CD8 T cells, critical for sustained immunity and immunotherapy response, we identify differentiation from Ccr6 to Ccr6 progenitors, shared between acute and chronic infections. ArchVelo provides a principled framework for modeling dynamic gene regulation and trajectory inference in multi-omic single-cell data across biological systems. - Source: PubMed
Publication date: 2026/06/06
Avdeeva MariaWalker Sarah Kvan der Veeken JorisRudensky Alexander YPritykin Yuri - Regulatory T cells (Tregs) infiltrate most tumors, and increased Treg infiltration is correlated with reduced survival in cancer patients. While Tregs suppress antitumor immunity, they are also integral for preventing harmful inflammation in non-tumor tissues, hindering the development of cancer therapeutic strategies targeting all Tregs systemically. Here, we used intratumoral (IT) delivery of diphtheria toxin (DT) in Foxp3DTR mice to deplete Tregs within tumor tissues while leaving peripheral Tregs intact. IT delivery of DT reduced Treg frequencies in the tumor, which promoted potent tumor control without autoimmunity. Interestingly, tumor control was principally mediated by CD4+ T cells, whereas CD8+ T cells only contributed when CD4+ T cells were absent. While conventional dendritic cells (cDCs) were required to clear tumors, either cDC1s or cDC2s alone were sufficient to promote tumor control. Distant secondary tumors, mimicking metastases, were also controlled by IT Treg ablation in the primary tumor. Mechanistically, IT Tregs suppressed antitumor T cell responses by blocking the acquisition and presentation of tumor antigen by cDC2s. Importantly, similar mechanisms of control were observed using a clinically translatable IT Treg-depleting anti-CCR8 antibody. Collectively, these findings reveal a distinct therapeutic strategy that leverages CD4+ T cells upon ablation of Tregs within tumors. - Source: PubMed
Publication date: 2026/06/02
Bockman AlissaZhang ChenyuGittins BrennaHung JessicaCampbell Timothy FMoreno Ayala Mariela ASaddier Axe DorothéeWeist Brian MDuPage Michel - Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide, increasingly driven by metabolic dysfunction-associated steatotic liver disease alongside viral and alcohol-related cirrhosis. The tolerogenic immune environment of the liver enables tumor immune escape, with regulatory T cells (Tregs) playing a central role. This review synthesizes human-focused evidence (tissues, blood, clinical cohorts, and single-cell/spatial studies) through September 2025 to define how Tregs are recruited, maintained, and functionally deployed in HCC. Across datasets, intratumoral effector-like Tregs (eTregs) expressing ICOS, CTLA-4, CCR8, and CD39/CD73 accumulate within tumors and co-localize with exhausted cytotoxic PD-1 CD8 T cells and suppressive myeloid cells. Recruitment is driven mainly by CCL20-CCR6 and CCL22/CCL17-CCR4 signaling, while CCR8 marks highly suppressive tumor-resident Tregs. Their persistence is supported by TGF-β, IL-10, IL-35, adenosine signaling, IL-2 sequestration, and metabolic adaptation. Spatial biomarkers, including ICOS/CCR8 eTreg density and CD8:Treg ratios, associate with prognosis and emerging immunotherapy responses. Etiology further shapes immune architecture: HBV-related HCC often forms Treg-exhausted T-cell niches around viral antigens, whereas MASLD/MASH promotes stromal and metabolic barriers that may reduce PD-(L)1 efficacy. Current treatments (PD-(L)1 blockade with anti-VEGF or CTLA-4, and some TKIs) intersect with Treg biology, while emerging strategies targeting CCR8, CCR4, ICOS, or the adenosine pathway aim to selectively disrupt intratumoral eTreg networks. This review underscores that an etiology-aware, spatial-biomarker framework may guide the integration of selective Treg targeting with PD-(L)1-based therapies in HCC. - Source: PubMed
Publication date: 2026/05/21
Liapopoulos DimitrisSarantis PanagiotisZogas GeorgiosTrifylli Eleni-MyrtoBousou Thaleia-EleftheriaKamitaki KonstantinaAnastasiou Ioanna AKokkali StefaniaMavromatis SotirisKoustas EvangelosElefsiniotis IoannisBiniari TheodoraKaramouzis Michalis V