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  • mProX™ Human CD28 Stable Cell Line

    [CAT#: S01YF-1023-PY221]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    CD Cell Lines

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    Product Information

    Target Family
    CD
    Target Protein Species
    Human
    Host Cell Type
    HEK293;CHO-K1;RPMI-8226
    Target Classification
    CD Cell Lines
    Target Research Area
    Cancer Research
    Related Diseases
    Classic Mycosis Fungoides; Sezary's Disease
    Gene ID
    Human:940
    UniProt ID
    Human:P10747

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    CD28 is a protein that plays a role in various applications. In the context of graft-versus-host disease (GVHD), CD28 is involved in sustaining T cell responses in target tissues, such as the liver and intestine. Its loss can lead to aberrant expression of PD-1 in T cells, decreased numbers of tissue-infiltrating PD-1+ T cells, and impaired maintenance of progenitor-like T cells. However, PD-1 blockade can restore the capacity of CD28-deficient T cells to mediate GVHD. CD28 is also required for protecting CD8+ T cells from PD-1 pathway-mediated suppression during GVHD. In addition, CD28 is important for the function of CAR-T cells, a type of immunotherapy for cancer. It is involved in the expansion, activation, and cytotoxicity of CAR-T cells. CD28 signaling is also associated with the immune response to vaccines. In a study on turbot fish, CD28 was found to be differentially expressed in kidney tissue after vaccination with an inactivated bivalent vaccine. Furthermore, CD28 is implicated in the interplay between SARS-CoV-2 and HIV. In individuals co-infected with these viruses, CD28 expression on T cells is dysregulated, leading to immune activation and altered T cell exhaustion. Overall, CD28 has important roles in immune responses, immunotherapy, vaccine responses, and viral infections.

    Protocols

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    FAQ

    chat Alex Jones (Verified Customer)

    Does CD28 signaling influence T cell adhesion? Jul 16 2022

    chat Patrick Liam (Creative Biolabs Scientific Support)

    CD28 signaling results in inhibition of Rap1 activity and decreased LFA-1-mediated adhesion, regulated by the recruitment of calcium-promoted Ras inactivator (CAPRI) to the plasma membrane. Jul 16 2022

    chat Skyler Davis (Verified Customer)

    How does CD28 interact with B7 ligands in T cells? Feb 26 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    B7 ligands expressed on T cells interact with CD28 in cis at membrane invaginations of the immunological synapse, suggesting cis-signaling as a mechanism for boosting T cell functionality. Feb 26 2023

    Published Data

    Fig.1 Knockdown of CD28 promotes myeloma cell death.

    Lentivral particles encoding shRNA specific for CD28, GAPDH, or empty vector (pLKO.1) were used to infect RPMI-8226 myeloma cells. The cells were then cultured for four days in full serum media. Annexin V staining was utilized to evaluate survival.

    Ref: Murray, Megan E., et al. "CD28-mediated pro-survival signaling induces chemotherapeutic resistance in multiple myeloma." Blood, The Journal of the American Society of Hematology 123.24 (2014): 3770-3779.

    Pubmed: 24782505

    DOI: 10.1182/blood-2013-10-530964

    Research Highlights

    Sayadmanesh, Ali. et al. "Characterization of CAR T Cells Manufactured Using Genetically Engineered Artificial Antigen Presenting Cells." Cell journal, 2023.
    The use of chimeric antigen receptor (CAR) T cell therapy has become a potential solution for various types of cancer treatment. With the aim to increase the accessibility of this therapeutic approach, there is a need to improve the manufacturing process in terms of cost and product quality. Proposed strategies for enhancing T cell expansion include the utilization of genetically engineered artificial antigen presenting cells (aAPC) that express a membrane-bound anti-CD3 for T cell activation. This study aimed to assess the efficiency, immunophenotype, and cytotoxicity of CAR T cells generated using this aAPC-mediated method.
    Sayadmanesh, Ali. et al. "Characterization of CAR T Cells Manufactured Using Genetically Engineered Artificial Antigen Presenting Cells." Cell journal, 2023.
    Pubmed: 37865876   DOI: 10.22074/cellj.2023.2001712.1304

    Xiu, Yunji. et al. "Transcriptome analysis of turbot (Scophthalmus maximus) kidney responses to inactivated bivalent vaccine against Aeromonas salmonicida and Edwardsiella tarda." Fish & shellfish immunology, 2023.
    Scophthalmus maximus, commonly known as Turbot, is a vital species for global aquaculture. However, its intensive farming is hindered by various diseases, with Aeromonas salmonicida and Edwardsiella tarda being the main causative agents. The development of an inactivated bivalent vaccine against these pathogens has shown promising results, with a relative percent survival (RPS) of 77.1%. To further understand the underlying protection mechanism, a study was conducted using RNA-seq to analyze the transcriptomic profile of the kidney tissue after immunization. The results show that a majority of the clean reads were mapped to the reference genome of S. maximus, and differentially expressed genes (DEGs) were enriched in important immune-related gene ontology terms. Furthermore, qRT-PCR analysis of selected DEGs confirmed the validity of the RNA-seq results. This study provides valuable insights into the immune mechanism of the inactivated bivalent vaccine against A. salmonicida and E. tarda in Scophthalmus maximus, that can aid in future research and development of effective disease prevention strategies.
    Xiu, Yunji. et al. "Transcriptome analysis of turbot (Scophthalmus maximus) kidney responses to inactivated bivalent vaccine against Aeromonas salmonicida and Edwardsiella tarda." Fish & shellfish immunology, 2023.
    Pubmed: 37858783   DOI: 10.1016/j.fsi.2023.109174

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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