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In vitro elimination of epidermal growth factor receptor-overexpressing cancer cells by CD32A-chimeric receptor T cells in combination with cetuximab or panitumumab. | LitMetric

AI Article Synopsis

  • Cetuximab and panitumumab are antibodies that target the human epidermal growth factor receptor (EGFR), but only cetuximab activates immune cells to kill cancer effectively through a process called antibody-dependent cellular cytotoxicity (ADCC).
  • This study focuses on comparing two types of T cells engineered with different receptors (CD32A and CD16) to see which is more effective at killing EGFR-positive cancer cells when combined with these antibodies.
  • The results show that CD32A-engineered T cells can effectively eliminate certain breast cancer cells when redirected by cetuximab or panitumumab, highlighting their potential in treating cancers that overexpress EGFR.

Article Abstract

Cetuximab and panitumumab bind the human epidermal growth factor receptor (EGFR). Although the chimeric cetuximab (IgG1) triggers antibody-dependent-cellular-cytotoxicity (ADCC) of EGFR positive target cells, panitumumab (a human IgG2) does not. The inability of panitumumab to trigger ADCC reflects the poor binding affinity of human IgG2 Fc for the FcγRIII (CD16) on natural killer (NK) cells. However, both human IgG1 and IgG2 bind the FcγRII (CD32A) to a similar extent. Our study compares the ability of T cells, engineered with a novel low-affinity CD32A -chimeric receptor (CR), and those engineered with the low-affinity CD16 -CR T cells, in eliminating EGFR positive epithelial cancer cells (ECCs) in combination with cetuximab or panitumumab. After T-cell transduction, the percentage of CD32A -CR T cells was 74 ± 10%, whereas the percentage of CD16 -CR T cells was 46 ± 15%. Only CD32A -CR T cells bound panitumumab. CD32A -CR T cells combined with the mAb 8.26 (anti-CD32) and CD16 -CR T cells combined with the mAb 3g8 (anti-CD16) eliminated colorectal carcinoma (CRC), HCT116 cells, in a reverse ADCC assay in vitro. Crosslinking of CD32A -CR on T cells by cetuximab or panitumumab and CD16 -CR T cells by cetuximab induced elimination of triple negative breast cancer (TNBC) MDA-MB-468 cells, and the secretion of interferon gamma and tumor necrosis factor alpha. Neither cetuximab nor panitumumab induced Fcγ-CR T antitumor activity against Kirsten rat sarcoma (KRAS)-mutated HCT116, nonsmall-cell-lung-cancer, A549 and TNBC, MDA-MB-231 cells. The ADCC of Fcγ-CR T cells was associated with the overexpression of EGFR on ECCs. In conclusion, CD32A -CR T cells are efficiently redirected by cetuximab or panitumumab against breast cancer cells overexpressing EGFR.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8711771PMC
http://dx.doi.org/10.1002/ijc.32663DOI Listing

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