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Application: / Assess the impact of B2M knockout on iPSC derived cardiomyocyte function./ Assess the impact of B2M knockout in cell therapy research and development.
Background: The discovery of the Yamanaka factors has enabled the reprogramming of mature human somatic cells to induced pluripotent stem cells (iPSCs) with the ability to differentiate along the three germlines lineages involved in human development (endo-, meso- and ectoderm). The impact of this discovery has been most profound in research involving terminally differentiated, non-proliferating cell types which have traditionally been difficult to access. One of the major causes of the death and burden on the health systems in the developed world are cardiovascular diseases and human iPSC-derived cardiomyocytes have furthered our understanding of human cardiac development, congenital heart diseases and mechanisms of drug-induced cardiotoxicity. Importantly, human iPSC derived cardiomyocytes also serve as a source for cell therapies to repair damaged heart tissue. Several strategies are currently under clinical trial for cardiomyocyte cell-replacement therapies, including the transplantation of dissociated cells, engineered heart tissues patches and cardiac spheroids. The goal of any cardiac cell therapy is engraftment of the in vitro-generated cardiomyocytes onto the recipient’s heart and integration of structural and electrophysiological systems to support recipient cardiac function. Similar to whole-organ transplantation, iPSC derived cell therapies are subject to mechanisms of immune rejection, which can decrease the efficiency of cell engraftment and retention which impedes the therapeutic effect. B2M (Beta-2-Microglobulin) forms a heteromeric complex with HLA-A, HLA-B and HLA-C molecules to generate the functional Class I MHC molecule responsible for antigen presentation to T-Cells. Class I MHC molecules are present on the surface of all nucleated cells and play a role in the rejection of organs or allogenic cells during organ transplantation and cell therapy. B2M is one of several attractive targets to reduce the immunogenicity of iPS cell-derived allogenic cell therapies. While the current cardiomyocyte cell therapies undergoing clinical trial do not leverage hypoimmune edits to provide immune cloaking, several are under development in preclinical pipelines.
Description: The Human B2M Knockout iPSC-Derived Cardiomyocytes are non-diseased, non-proliferative human cardiomyocytes differentiated from B2M Knockout iPS Cell Line (#82161). The iPS cell line was generated using CRISPR/Cas9 technology to remove B2M (Beta-2-Microglobulin) gene expression. The B2M-targeting CRISPR/Cas9 editing reagents were delivered via transduction with B2M (Human) CRISPR/Cas9 Lentivirus (Non-Integrating) (#78341).
Host Cell Line: PBMC-derived, non-disease Human iPS Cell Line (XCells 30HU-002)
Mycoplasma Testing: The cell line has been screened to confirm the absence of Mycoplasma species.
Storage Stability: Cells are shipped in dry ice and should immediately be thawed or stored in liquid nitrogen upon receipt. Do not use a -80°C freezer for long term storage.
Supplied As: Each vial contains 5 x 106 cells in 1 ml of STEMdiff Cardiomyocyte Freezing Media (Stem Cell Technologies #05030)
Target: B2M
Uniprot: F5H6I0
Warnings: Avoid freeze/thaw cycles.
Biosafety Level: BSL-1
References: Cong L., et al., 2013 Science. 339(6121):819-23.Deuse T., et al., 2019 Nat Biotechnol (3):252-258.Eschenhagen T., et al., 2022 J. Mol Cell Cardiol 163: 106-117.Gerace D., et al., 2023 Cell Reports Medicine 4: 100879Jinek M., et al., 2012 Science. 337(6096):816-21.Lian X., et al., 2012, PNAS 109(27): E1848-E1857.Lanza R., et al., 2019 Nat Rev Immunol 19: 723-733.Kirkeby, A., et al., 2025 Cell Stem Cell 32(1):10 – 37.Mali P., et al., 2013 Science. 339(6121):823-6.Mordwinkin., et al., 2013, J Cardiovasc Transl Res 6: 22-30.Musunuru K., et al., 2018 Circ Genom Precis Med 11: e000043.Takahashi K., et al., 2007 Cell. 131(5):861–872.Yamanaka S., et al., 2012, Cell Stem Cell 10: 678-684.Yang L., et al., 2013 Nucleic Acids Res. 41(19):9049-61.
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