Journal
MABS
Volume 5, Issue 4, Pages 587-594Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/mabs.25077
Keywords
ADCC; transfection; mouse; CD16; human; lymphocyte; NK; xenogenic
Categories
Funding
- INSERM
- CANCEROPOLE Grand Ouest
- Ligue Regionale contre le Cancer
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To take advantage of the large number of well-characterized mouse immunoglobulins (IgGs) for the study of antibody-dependent cell-mediated cytotoxicity (ADCC) in human cells, we armed human cytotoxic lymphocytes with a mouse receptor for the Fc portion of IgG antibodies. The human -92 natural killer cell line was transduced with a mouse receptor gene (mCD16), which was stably expressed on the cell surface (referred to as NK-92(mCD16)). When tested against a B-lymphoblastoid cell line (BLCL) coated with mouse anti-CD20 IgG1, IgG2a or IgG2b monoclonal antibodies (mAbs), the newly expressed mouse Fc receptor enabled the NK-92(mCD16) cells to kill the BLCL by ADCC. Next, using the NK-92(mCD16) we compared mouse mAbs directed at B lineage specific CD antigens for their ability to induce ADCC against human Epstein-Barr virus- infected B lymphoblastoid (for anti-CD19, -CD20 and -CD21) or against myeloma (for anti-CD38 and -CD138) target cells. Our results demonstrated that the NK-92(mCD16) assay allows convenient and sensitive discrimination of mouse mAbs for their ability to mediate ADCC in a human cellular system. In addition, our results provide examples of dissociation between opsonization and target cell killing through ADCC. These murinized human effector cells thus represent a convenient cellular tool for the study of ADCC.
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