2009
DOI: 10.1016/j.imlet.2008.10.009
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Knockdown of human bid gene expression enhances survival of CD8+ T cells

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Cited by 11 publications
(4 citation statements)
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“…Multiple reports have underscored the importance of knocking down apoptotic genes (e.g. Bim, Bid, Bax, FasL) to improve T cell longevity [58,[271][272][273][274][275][276][277]. For example, blocking Bid expression in CD8 + T cells using virally expressed siRNAs significantly reduced Fas-induced apoptosis and enhanced T cell survival in low IL-2 concentrations [272].…”
Section: Ex Vivo Therapeutic Potential Of Sirna In Cancer Immunotherapymentioning
confidence: 99%
“…Multiple reports have underscored the importance of knocking down apoptotic genes (e.g. Bim, Bid, Bax, FasL) to improve T cell longevity [58,[271][272][273][274][275][276][277]. For example, blocking Bid expression in CD8 + T cells using virally expressed siRNAs significantly reduced Fas-induced apoptosis and enhanced T cell survival in low IL-2 concentrations [272].…”
Section: Ex Vivo Therapeutic Potential Of Sirna In Cancer Immunotherapymentioning
confidence: 99%
“…Although many antitumor agents have been used to target the proteins involved in apoptosis to induce cancer cell death or enhance the sensitivity of cancer cells to certain cytotoxic drugs or radiation, targeting of proapoptotic proteins have not been considered enough in CAR T cell therapy to make more persistent CAR T cells. There are many investigations underscoring that targeting proapoptotic protein in T cells can improve T cell longevity (118)(119)(120)(121)(122)(123)(124). Thus, it seems that knocking down or knocking out of proapoptotic proteins such as Bim and/or Bid, by shRNA and siRNA or CRISPR/Cas9 respectively can lead to increased survival of CAR T cells in a similar way to tumor cells which acquire resistance to apoptosis through downregulation or mutation of proapoptotic proteins.…”
Section: Knocking Down Of Proapoptotic Molecules and Overexpression Omentioning
confidence: 99%
“…T-cell functions can be significantly improved by genetic modifications such as downregulation of BH3-interacting domain death agonist (BID) [72, 73] or upregulation of BCL-XL and BCL-2 [74, 75], insertion of CTLA4 mutant gene [76], transfection of human c-fms gene for responding to colony-stimulating factor-1 (CSF-1) [77], transduction of C-X-C chemokine receptor type 2 (CXCR2), C-C chemokine receptor type 4 (CCR4) or CCR2B for better migration [78], and modification to express PD1-CD 28 chimaera to overcome immune suppression [79]. In addition, T cells can be equipped with genes that encode receptors capable of recognizing cancer-specific antigen.…”
Section: T-cell-based Cell Transfermentioning
confidence: 99%