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Montalvo, M. J.

Publications and source records attributed to Montalvo, M. J..

2 recordsLinked to original sources

Engineering non-cytotoxic delivery of proteins by T cells via fusion to NPC2

Engineering cellular therapeutics by programming T cells has great potential in immunology. The primary mechanism employed by T cells for the specific transfer of proteins at the immunological synapse is via the lysosomal perforin pathway that facilitates the transfer of cytotoxic granzymes leading to apoptosis in target cells. Facilitating the delivery of non-cytotoxic proteins through perforin oligomers will dramatically expand the range of protein cargos that T cells can traffic to the target cells. Here, we have identified the intralysosomal protein, NPC2, as a chaperone that can facilitate the delivery of T-cell derived reporter proteins through perforin pores at the immunological synapse. Structural and biophysical considerations suggested that NPC2 could traverse through perforin pores and in vitro experiments confirmed the transport of purified NPC2 through perforin pores on cell membranes. To characterize the ability of NPC2 to facilitate the transfer of payloads in T cells, we constructed NPC2-mCherry fusion proteins in T cells. Using confocal microscopy and flow cytometry, we confirmed the colocalization of the NPC2 fused protein with lytic granules and the transfer of the fluorescent protein payload from T cells to target cells in co-culture experiments. The NPC2 fusion enabled the localization of mCherry to secretory lysosomes in mouse TCR CD8+ T cells and human CD4+ and CD8+ chimeric antigen receptor (CAR) T cells. These results illustrate that by using NPC2 as a molecular chaperone, the NPC2-perforin pathway can be exploited as a programmable molecular delivery system for cell-based therapies.

immunology↗

Integrated single-cell functional and molecular profiling of extracellular vesicle secretion in metastatic breast cancer

Extracellular vesicles (EVs) regulate the tumor microenvironment by facilitating transport of biomolecular cargo including RNA, protein, and metabolites. The biological effects of EV-mediated transport have been studied using supra-physiological concentrations of EVs, but the cells that are responsible for EV secretion and the mechanisms that support EV secretion are not well characterized. We developed an integrated method based on arrays of nanowells to identify individual cells with differences in EV secretion and used an automated robot to perform linked single-cell RNA-sequencing on cloned single cells from the metastatic breast cancer cell line, MDAMB231. Gene expression profiles of clonal cells with differences in EV secretion were analyzed, and a four-gene signature of breast cancer EV secretion was identified: HSP90AA1, HSPH1, EIF5, and DIAPH3. We functionally validated this gene signature by testing it across different cell lines with different metastatic potential demonstrating that the signature correlated with levels of EV secretion. Analysis of the TCGA and METABRIC datasets showed that this signature is associated with poor survival, more invasive breast cancer types, and reduced CD8+ T cell infiltration in human tumors. We anticipate that our method for directly identifying the molecular determinants of EV secretion will have broad applications across cell types and diseases.

cancer biology↗