Cytokine-induced killer (CIK) cells bound with anti-CD3/anti-CD133 bispecific antibodies target CD133(high) cancer stem cells in vitro and in vivo
© 2013.
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 149(2013), 1 vom: 18. Okt., Seite 156-68 |
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| Auteur principal: | |
| Autres auteurs: | , , , , , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2013
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Bispecific antibody (BsAb); CD133 CD3; Cancer stem cell (CSC); Cytokine induced killer (CIK) cells; AC133 Antigen Antibodies, Bispecific Antigens, CD plus... |
| Résumé: | © 2013. CD133 is a common marker of cancer stem cells (CSCs). We generated an anti-CD3/anti-CD133 bispecific antibody (BsAb) and bound it to the cytokine-induced killer (CIK) cells as effector cells (BsAb-CIK) to target CD133(high) CSCs. The killing of CD133(high) pancreatic (SW1990) and hepatic (Hep3B) cancer cells by the BsAb-CIK cells was significantly (p<0.05) higher than the killing by the parental CIK or by CIK cells bound with anti-CD3 (CD3-CIK) without CD133 targeting. In nude mice, the BsAb-CIK cells inhibited CD133(high) tumor growth significantly (p<0.05) more than that by CIK or CD3-CIK cells, or by the BsAb alone. BsAb-CIK cells co-cultured with CD133(high) cells produced significantly (p<0.05) higher amount of IFN-γ. Treatment with the BsAb-CIK cells significantly downregulated the expression of S100P and IL-18bp, but upregulated STAT1. The findings may help with the development of novel immunotherapies for patients with cancer containing CD133(high) CSCs by selectively targeting this cell population |
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| Description: | Date Completed 12.11.2013 Date Revised 22.12.2020 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2013.07.006 |