Myeloid derived suppressor cells (MDSC) have recently been identified as a target site for immunotherapy techniques due to their role in regulating antitumor immune response and tumor progression. Tumor-associated MDSC are characterized by an overexpression of oxidative machinery which is responsible for their observed suppression of innate immune responses. This enzymatic machinery has been shown to effectively degrade carbonaceous nanoparticles providing an avenue for targeted drug delivery directly to MDSC. We illustrate the use of gold-decorated nitrogen doped carbon nanotubes (Au-NCNC) for the <i>in vivo</i> delivery of paclitaxel to MDSC resulting in tumor growth inhibition over a 3-week period. The enzymatic degradation of carbon nanotubes and paclitaxel payload were explored illuminating a potential mechanism of MDSC to prevent effective chemotherapy treatment due to degradation of paclitaxel. Carbon nanotubes therefore represent an attractive drug delivery vehicle due to their ability to scavenge the oxidative potential of MDSC allowing for prolonged interaction of paclitaxel payload with the tumor microenvironment. Furthermore, <i>in vivo</i> systemic administration of paclitaxel by Au-NCNC was found to affect MDSC populations in the spleen and liver illustrating a conditioning of the immune system for proposed prevention of metastatic cancer growth. The resulting effects on tumor growth and MDSC population were not observed from systemic administration of free paclitaxel illustrating the necessity of a drug delivery vehicle with enzymatic scavenging potential for improving therapeutic efficacy. The results of this investigation illustrate how the oxidative machinery of MDSC is paramount towards their observed immune suppression and can be exploited for enhanced immunotherapy techniques.

Exploiting enzymatic activity of myeloid-derived suppressor cells for payload delivery and enhanced therapeutic efficacy

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.