| Field | Specification |
|---|---|
| Mfr No | |
| Accession Number | |
| Alternative Names | BY55, NK1, NK28 |
| Product Type | |
| Shipping | |
| Species | |
| Storage |
Scientific Background
CD160 is a glycosylphosphatidylinositol (GPI)-anchored protein member of the Ig superfamily that is expressed at the cell surface and highly restricted to circulating NK and T cells. Binding of CD160 to both classical and non-classical MHC I enhances NK and CD8+ CTL functions. However, engagement of CD160 by the Herpes Virus Entry Mediator (HVEM / TNFRSF14) was shown to mediate inhibition of CD4+ T-cell proliferation and TCR-mediated signaling. HVEM protein is a bimolecular switch that binds both co-stimulatory LT-α/LIGHT and co-inhibitory receptors CD160/BTLA. The binding of coinhibitory receptors CD160 and/or BTLA on T cells with HVEM expressed on DC or Tregs transduces negative signals into T cells that are counterbalanced by costimulatory signals delivered after direct engagement of HVEM on T cells by LIGHT expressed on DC or more likely, on other activated T cells (T-T cell cooperation). HVEM was also shown to be expressed in the majority of cultured melanoma cell lines and metastatic melanoma samples. The predominance of the interaction of HVEM with CD160 and BTLA over the HVEM/LIGHT pathway or vice versa might be the result of differences in ligand/receptor affinity and the differential expression pattern of these molecules on cell types at different stages of cell differentiation. LIGHT, BTLA, and CD160 have substantially different binding affinities and occupy spatially distinct sites upon interaction with the HVEM receptor, which enables HVEM to function as a molecular switch. The net effect of the LIGHT/HVEM and HVEM/BTLA/CD160 interaction, when these different receptors and ligands are simultaneously present, determines the outcome of the response. CD160/HVEM interaction plays a key role in the regulation of inflammatory, autoimmune, and antitumor responses, and is an important target for cancer immunotherapy drug discovery. The interaction of CD160 on tumor specific T cells and HVEM on melanoma cells resulted in T cell inhibition, which could be reversed by treatment with anti-CD160 blocking antibody. Therapeutically targeting CD160 and HVEM remains a focus for in pre-clinical studies as the bidirectional signaling pathways of CD160/BTLA/HVEM and HVEM/LIGHT are further elucidated.
Product Description
Immunotherapy Immune CheckpointsRecombinant Jurkat T cell expressing firefly luciferase gene under the control of NFAT response elements with constitutive expression of human CD160. CD160 is a GPIanchored glycoprotein member of the Ig superfamily, also known as BY55, NK1, and NK28. GenBank Accession # NM_007053.
Product Specifications
| Host Cell Line | Jurkat (clone E6-1) |
|---|---|
| Host Species | Human t lymphoblast, suspension |
| Transfection Method | Electroporation |
| Supplied As | Each vial contains 2 x 10^6 cells in 1 ml of 10% DMSO |
| Harmonized Tariff Code | 3002-5900 |
Quality Control & Validation
✓ Mycoplasma-TestedThe cell line has been screened using the PCR-based Venor™GeM Mycoplasma Detection kit (Sigma-Aldrich, #MP0025) to confirm the absence of Mycoplasma species.
Usage Notes
See data sheet for detailed culturing and assay protocol.
Safety & Handling
⚠ Avoid freeze/thaw cycles.
Regulatory Information
License Disclosure
Related Products
Related Products: Cat. #60190, 79551, 60690, 60184, 79796
Required Accessories: Cat. #60184,79796,60690,60190
This product is engineered on a Jurkat (clone E6-1) background (Human origin). The Jurkat (clone E6-1) host was selected for its compatibility with stable transfection and the target pathway or assay type. Consult the product datasheet for passage number guidance and recommended culture media.
This product is classified as BSL-1. Standard microbiological practices (gloves, lab coat, eye protection) are sufficient. No specialized containment facility is required beyond a clean bench. Consult your institutional IBC for GMO registration requirements.
Yes. The cell line has been screened using the PCR-based Venor™GeM Mycoplasma Detection kit (Sigma-Aldrich, #MP0025) to confirm the absence of Mycoplasma species. We recommend that you independently confirm mycoplasma-negative status after receipt and periodically during routine culture using a validated detection kit.
Store this product at Liquid Nitrogen. Specifically: Immediately upon receipt, store in liquid nitrogen. Transfer cells from dry-ice shipping to the recommended storage immediately upon receipt. Avoid repeated freeze-thaw cycles, which reduce viability and may alter expression characteristics.
Yes, a license is required (Yes). Purchase of this cell line grants a time-limited research-use license for use in your immediate laboratory only. This license does not permit redistribution, sub-licensing, transfer to other institutions, or commercial use. Refer to the License Disclosure section on this page or contact BPS Bioscience for details regarding modifications or commercial licensing.
This stable cell line was generated using Electroporation for transgene delivery into the parental host. The stably integrated cells were selected using the appropriate resistance marker and verified for expression prior to cryopreservation.
Can't find the cell line you need—or require a custom engineered model for your study? We offer end-to-end support for diverse research needs, including:
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- del Rio, M.L., et al. HVEM/LIGHT/BTLA/CD160 co-signaling pathways as targets for immune regulation. Journal of Leukocyte Biology. 2010; 87(2): 223-35 2. Quan L. et al. BTLA marks a less cytotoxic T-cell subset in diffuse large B-cell lymphoma with high expression of checkpoints. Exp Hematol. 2018 Feb 3; 60: 47-56.
- Torphy RJ, et al. Newly Emerging Immune Checkpoints: Promises for Future Cancer Therapy. Int J Mol Sci. 2017 Dec 6;18(12): E2642. Review.
- Spodzieja M, et al. Design of short peptides to block BTLA/HVEM interactions for promoting anticancer T-cell responses. PLoS One. 2017 Jun 8;12(6): e0179201 5. Cara L Haymaker et al. BTLA marks a less-differentiated tumor-infiltrating lymphocyte subset in melanoma with enhanced survival properties. OncoImmunology. August 2015; 4(8): e1014246.
- Antonia SJ et al. Immunotherapy: Beyond Anti-PD-1 and Anti-PD-L1 Therapies. Am Soc Clin Oncol Educ Book. 2016; 35: e450-8 7. Zhang T, et al. Knockdown of HVEM, a Lymphocyte Regulator Gene, in Ovarian Cancer Cells Increases Sensitivity to Activated T Cells. Oncol Res. 2016; 24(3): 189-96 8. Lan X, et al. Increased BTLA and HVEM in gastric cancer are associated with progression and poor prognosis. Onco Targets Ther. 2017 Feb 16; 10: 919-926.
- Zhao Q, et al. BTLA identifies dysfunctional PD-1-expressing CD4+ T cells in human hepatocellular carcinoma. Oncoimmunology. 2016 Nov 8; 5(12): e1254855.
- Boice M, et al. Loss of the HVEM Tumor Suppressor in Lymphoma and Restoration by Modified CAR-T Cells. Cell. 2016 Oct 6; 167(2):405-418 11. Shui, J-W. and Kronenberg, M. HVEM is a TNF Receptor with Multiple Regulatory Roles in the Mucosal Immune System. Immune Network April, 2014; 14(2): 67-72.
- Steinberg, M., et al. The Signaling Networks of the HVEM/BTLA in Immune Regulation. Immunol Rev. 2011 November; 244(1): 169-187
