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• W2159027903 abstract "Abstract Improving effector T-cell functions is highly desirable for preventive or therapeutic interventions of diverse diseases. Signal transducer and activator of transcription 3 (Stat3) in the myeloid compartment constrains Th1-type immunity, dampening natural and induced antitumor immune responses. We have recently developed an in vivo small interfering RNA (siRNA) delivery platform by conjugating a Toll-like receptor 9 agonist with siRNA that efficiently targets myeloid and B cells. Here, we show that either CpG triggering combined with the genetic Stat3 ablation in myeloid/B cell compartments or administration of the CpG-Stat3siRNA drastically augments effector functions of adoptively transferred CD8+ T cells. Specifically, we show that both approaches are capable of increasing dendritic cell and CD8+ T-cell engagement in tumor-draining lymph nodes. Furthermore, both approaches can significantly activate the transferred CD8+ T cells in vivo, upregulating effector molecules such as perforin, granzyme B, and IFN-γ. Intravital multiphoton microscopy reveals that Stat3 silencing combined with CpG triggering greatly increases killing activity and tumor infiltration of transferred T cells. These results suggest the use of CpG-Stat3siRNA, and possibly other Stat3 inhibitors, as a potent adjuvant to improve T-cell therapies. Cancer Res; 70(19); 7455–64. ©2010 AACR." @default.
• W2159027903 created "2016-06-24" @default.
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• W2159027903 date "2010-09-29" @default.
• W2159027903 modified "2023-10-11" @default.
• W2159027903 title "Targeting Stat3 in the Myeloid Compartment Drastically Improves the <i>In vivo</i> Antitumor Functions of Adoptively Transferred T Cells" @default.
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• W2159027903 doi "https://doi.org/10.1158/0008-5472.can-10-0736" @default.
• W2159027903 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3058618" @default.
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