ADCP Bioassay Effector Cell FcgammaRI (CD64)/NFAT Luciferase Reporter Jurkat Cell Line

ADCP Bioassay Effector Cell FcgammaRI (CD64)/NFAT Reporter Jurkat Cell Line is a Jurkat T cell line engineered to express firefly luciferase under the control of NFAT (nuclear factor of activated T cells) response elements, and human FcgammaRI (Fc-gamma receptor 1), also known as CD64. This cell line was functionally validated in a co-culture assay using antigen-expressing cells in the presence of a relevant antibody. Figure 1: Illustration of the mechanism of action of ADCP Bioassay Effector Cell FcgammaRI (CD64)/NFAT Luciferase Reporter Jurkat Cell Line. ADCP Bioassay Effector Cell FcgammaRI (CD64)/NFAT Luciferase Reporter Jurkat cells are used as effector cells. The effector cells are co-cultured in the presence of target cells and an antibody of interest. The antibody binds to the target antigen on the target cell whereas its Fc portion binds to FcgammaRI on the cell surface of the effector cell, cross-linking the effector and target cells. Engagement of FcgammaRI leads to the activation of the NFAT pathway in the effector cells. Luciferase activity is proportional to the activation of the ADCP cascade. Interested in screening and profiling inhibitors, blocking antibodies, or activators of FcgammaRI (CD64) without the need to purchase and license the cell line? Check out our Cell Signaling Pathway Screening. Antibody-dependent cell-mediated phagocytosis (ADCP) is an important mechanism to consider during antibody drug development. FcgammaRI (Fc gamma receptor 1), also known as CD64, is found in macrophages and monocytes, and its expression can be induced in polymorphonuclear leukocytes by IFNg (interferon gamma) and GCSF (granulocyte colony-stimulating factor). Multivalent IgG immune complexes (ICs) promote receptor clustering and activation of intracellular signaling through phosphorylation of ITAMs (immunoreceptor tyrosine-based activation motifs), leading to phagocytosis via Rac-GEFs (guanine exchange factors). This mechanism of action has contributed to the success of rituximab (anti-CD20 antibody) in the treatment of chronic lymphocytic leukemia (CCL). However, an overactivation of FcgammaRI can result in chronic inflammation and autoimmune disorders, such as SLE (systemic lupus erythematosus), ITP (immune thrombocytopenia) and RA (rheumatoid arthritis). Leveraging FcgammaRI properties can be beneficial in cancer therapy, while blocking its activation is a promising therapeutic approach for autoimmune disorders.