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HEK293/Human CCR8 Stable Cell Line

For research use only.

  1. Genetically modified cell lines best reflect MOA (Mechanism of Action)
  2. Higher activity and larger assay window for robust and reproducible cell-based bioassay
  3. Comprehensive application data to support assay development and validation
  4. Full tracible record, stringent quality control and validated cell passage stability
  5. Parental cell line legally obtained from internationally recognized cell resource bank and commercially licensed
  6. Global commercial license assistance whenever regulatory filing is required

描述(Description)

The HEK293/Human CCR8 Stable Cell Line was engineered to express full length human CCR8 (Gene ID: 1237), used to mimic cancer target cells. Surface expression of human CCR8 was confirmed by flow cytometry.

应用说明(Application)

• Useful for cell-based CCR8 binding assay

生长特性(Growth Properties)

Adherent

筛选标记(Selection Marker)

Hygromycin B (20 μg/mL)

培养基(Complete Growth Medium)

DMEM + 10% FBS

冻存液(Freeze Medium)

Serum-free cell cryopreservation medium

装量(Quantity)

1 vial contains at least 5×10^6 cells in 1 mL serum-free cryopreservation medium

存储(Storage)

Frozen in liquid nitrogen.

支原体检测(Mycoplasma Testing)

Negative

无菌检测(Sterility Testing)

Negative

使用说明(Instructions for Use)

See data sheet for detailed culturing and assay protocol.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

Receptor Assay

CCR8 FACS

Expression analysis of human CCR8 on HEK293/Human CCR8 Stable Cell Line by FACS.
Cell surface staining was performed on HEK293/Human CCR8 Stable Cell Line or negative control cell using anti-human CCR8 antibody followed by staining with PE anti-human IgG antibody.

Protocol

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背景(Background)

This entry represents CC chemokine receptor 8 (CCR8), which it is expressed predominantly in lymphoid tissues and has also been found in glomerular podocytes and human umbilical vein endothelial cells (HUVECs). CCR8 is associated with Th2 lymphocytes, which are critical for allergy, and has a role in lymphocyte activation, migration, proliferation and differentiation and in allergic diseases. CCR8 binds to CCL1 (also known as I-309) and to CCL16 (also known as liver expressed chemokine). It also exhibits a high affinity for three chemokines of viral origin: vMIP-I, vMIP-II and vMCC-I.

Limited Use&License Disclosure

BY USE OF THIS PRODUCT, RESEARCHER AGREES TO BE BOUND BY THE FOLLOWING TERMS OF LIMITED USE OF THIS CELL LINE PRODUCT.

  1. If the researcher is not willing to accept the terms of limited use of this cell line product, and the product is unused, ACRO will accept return of the unused product.
  2. Researchers may use this product for research use only, no commercial use is allowed. "Commercial use" means any and all uses of this product and derivatives by a party for profit or other consideration and may include but is not limited to use in: (1) product manufacture; and (2) to provide a service, information or data; and/or resale of the product or its derivatives, whether or not such product or derivatives are resold for use in research.
  3. This cell line is neither intended for any animal or human therapeutic purposes nor for any direct human in vivo use . You have no right to share, modify, transfer, distribute, sell, sublicense, or otherwise make the cell line available for use to other researchers, laboratories, research institutions, hospitals, universities, or service organizations.
  4. ACROBIOSYSTEMS MAKES NO WARRANTIES OR REPRESENTATIONS OF ANY KIND, EITHER EXPRESSED OR IMPLIED, WITH RESPECT TO THE SUITABILITY OF THE CELL LINE FOR ANY PARTICULAR USE.
  5. ACROBIOSYSTEMS ACCEPTS NO LIABILITY IN CONNECTION WITH THE HANDLING OR USE OF THE CELL LINE.
  6. Modifications of the cell line, transfer to a third party, or commercial use of the cell line may require a separate license and additional fees. Please contact order.cn@acrobiosystems.com for further details.

 

前沿进展

Macrophage-derived CCL1 targets CCR8 receptor in hepatic stellate cells to promote liver fibrosis through JAk/STAT pathway
Diao, Li, Zhang et al
Biochem Pharmacol (2025)
Abstract: Liver fibrosis is caused by liver injury resulting from the wound healing response. According to recent research, the primary factor responsible for liver fibrosis is the activation of hepatic stellate cells (HSCs). C-C motif chemokine ligand 1 (CCL1) is one of several chemokine genes clustered on chromosome 17, which is involved in immune regulation and inflammatory processes. However, the role of CCL1 in liver fibrosis has not been reported. We found that CCL1 secreted by macrophages can target and activate the receptor protein C-C motif chemokine receptor 8 (CCR8) of HSCs, accelerating liver fibrosis progression by activating the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling pathway. This suggested that the CCL1-mediated regulation of CCR8 is an important event in liver fibrosis progression. In conclusion, this study identified a novel signalling axis, the CCL1/CCR8/JAK/STAT pathway, which regulates the activation and apoptosis of HSCs, thus providing a novel therapeutic strategy for liver fibrosis.Copyright © 2025. Published by Elsevier Inc.
A multi-omics analysis of effector and resting treg cells in pan-cancer
Chalepaki, Gkoris, Chondrou et al
Comput Biol Med (2025) 189, 110021
Abstract: Regulatory T cells (Tregs) are critical for maintaining the stability of the immune system and facilitating tumor escape through various mechanisms. Resting T cells are involved in cell-mediated immunity and remain in a resting state until stimulated, while effector T cells promote immune responses. Here, we investigated the roles of two gene signatures, one for resting Tregs (FOXP3 and IL2RA) and another for effector Tregs (FOXP3, CTLA-4, CCR8 and TNFRSF9) in pan-cancer. Using data from The Cancer Genome Atlas (TCGA), The Cancer Proteome Atlas (TCPA) and Gene Expression Omnibus (GEO), we focused on the expression profile of the two signatures, the existence of single nucleotide variants (SNVs) and copy number variants (CNVs), methylation, infiltration of immune cells in the tumor and sensitivity to different drugs. Our analysis revealed that both signatures are differentially expressed across different cancer types, and correlate with patient survival. Furthermore, both types of Tregs influence important pathways in cancer development and progression, like apoptosis, epithelial-to-mesenchymal transition (EMT) and the DNA damage pathway. Moreover, a positive correlation was highlighted between the expression of gene markers in both resting and effector Tregs and immune cell infiltration in adrenocortical carcinoma, while mutations in both signatures correlated with enrichment of specific immune cells, mainly in skin melanoma and endometrial cancer. In addition, we reveal the existence of widespread CNVs and hypomethylation affecting both Treg signatures in most cancer types. Last, we identified a few correlations between the expression of CCR8 and TNFRSF9 and sensitivity to several drugs, including COL-3, Chlorambucil and GSK1070916, in pan-cancer. Overall, these findings highlight new evidence that both Treg signatures are crucial regulators of cancer progression, providing potential clinical outcomes for cancer therapy.Copyright © 2025. Published by Elsevier Ltd.
Design and application of CCR8 antagonists
Van Loy, Schols, De Jonghe
Future Med Chem (2025)
Selective depletion of CCR8+Treg cells enhances anti-tumor immunity of cytotoxic T cells in lung cancer via dendritic cells
Chen, Wang, Tang et al
J Thorac Oncol (2025)
Abstract: Accumulation of regulatory T (Treg) cells, an immunosuppressive population, limits the efficacy of immunotherapy in non-small cell lung cancer (NSCLC). C-C Motif Chemokine Receptor 8 (CCR8) is selectively expressed in tumor-infiltrating Treg cells and, thus considered an ideal target. Across four NSCLC-bearing mice models, the combination of CCR8 antibody and programmed cell death protein-1 (PD1) inhibitor significantly reduced tumor growth without obvious mouse body weight drops and systemic cytokine storm. The single-cell RNA and T-cell receptor sequencing analysis demonstrated that anti-CCR8 therapy synergizes with PD1 blockade by remodeling the tumor microenvironment and disrupting CCR8+Treg - CCL5+ dendritic cells (DC) interaction. Mechanistically, therapeutic depletion of CCR8+Treg cells combined with PD1 inhibitor extremely increased interleukin-12 secretion by the JAK-STAT pathway activation on CCL5+ DCs, thereby promoting cytotoxic activity of CD8+ T cells. The therapeutic potential of the CCR8 antibody LM-108 in combination with immunotherapy was observed in clinical patients with advanced NSCLC. Overall, CCR8 expression on tumor-infiltrating Treg cells is correlated with immunosuppressive function on DCs and CD8+ T cells, thus impeding anti-tumor immunity.Copyright © 2025. Published by Elsevier Inc.
Showing 1-4 of 553 papers.
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CCR8靶点信息
英文全称:C-C chemokine receptor type 8
中文全称:CC趋化因子受体8型
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:14详情
最高研发阶段:临床二期
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