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Cat. No. ARG36840

B2M Knockout TE1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The B2M Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with disrupted B2M in the human TE1 esophageal squamous carcinoma cell line. Loss of beta-2-microglobulin abrogates MHC class I surface expression, impairing CD8+ T cell recognition and enhancing susceptibility to NK cell cytotoxicity, mimicking immune evasion in cancer. Regulated by IFNG, STAT1, and NF-kB, and interacting with HLA-A and the peptide loading complex (TAP1, tapasin), this model enables tumor immunology studies, including T cell/NK cell assays, immunotherapy screening, and antigen presentation research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    TE1

    Gene Name

    B2M

    Gene Identifier

    NCBI Gene ID 567

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The B2M Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout pool derived from the human TE1 esophageal squamous cell carcinoma line, with targeted disruption of the B2M gene. This heterogeneous population eliminates functional beta-2-microglobulin, providing a loss-of-function model for MHC class I studies. The polyclonal format avoids clonal selection artifacts and preserves cellular diversity, making it suitable for population-level immune assays and tumor biology research.

The TE1 cell line originates from a well-differentiated human esophageal squamous carcinoma and is widely used in cancer research. These adherent epithelial cells retain tumorigenic properties and interferon-gamma responsiveness, offering a relevant platform for investigating immune evasion mechanisms in esophageal cancer.

B2M encodes beta-2-microglobulin, which stabilizes MHC class I heavy chains (HLA-A, HLA-B, HLA-C) for antigen presentation to CD8+ T cells. Within the endoplasmic reticulum, beta-2-microglobulin associates with the peptide loading complex??including TAP1, TAP2, tapasin, calreticulin, and ERp57??to facilitate peptide loading and MHC class I transport. B2M expression is regulated by interferon-gamma (IFNG) via STAT1 and IRF1, as well as by NF-kB and TNF signaling. Disruption of B2M abrogates MHC class I surface expression, impairing CD8+ T cell recognition and promoting immune evasion, yet may enhance NK cell cytotoxicity due to absent inhibitory KIR and LILR interactions.

In TE1 cells, B2M knockout recapitulates MHC class I loss, a frequent immune evasion strategy in esophageal squamous cell carcinoma that correlates with poor prognosis. This model enables dissection of tumor-immune dynamics, including CD8+ T cell evasion and NK cell sensitization, facilitating studies on the balance between adaptive and innate immune pressures in the tumor microenvironment.

Applications include flow cytometry for MHC class I validation, western blotting and RT-qPCR for B2M expression, and co-culture cytotoxicity assays with CD8+ T cells or NK cells. The cells are also suitable for IFN-gamma stimulation tests and immunopeptidomics to interrogate antigen presentation alterations. Researchers can use this model for screening immune checkpoint inhibitors or novel immunotherapies targeting MHC class I-independent pathways. For further details or to request a quote, please contact Ascent Research.

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