Volume 3 Issue 4, April 2019

An antibody-modified nanoparticle encapsulating a pH-sensitive taxane prodrug, and targeting an overexpressed receptor in tumours, improves the tolerability and anticancer efficacy of the active drug in multiple animal models.

Nanoparticle sensors of the activity of the protease granzyme B detect early T-cell-mediated rejection of transplanted skin grafts in mice via the release of a proteolytically cleaved fluorescence reporter that filters into urine.

Depletion of cells expressing the cell-membrane protein programmed cell-death protein-1 using an antibody-based toxin delays the onset of disease in a mouse model of diabetes and reverses paralysis in mice with experimental autoimmune encephalomyelitis, without compromising physiological immunity.

Enhanced lysosomal degradation of the transmembrane protein programmed cell-death protein-1 ligand in tumour cells, enabled by blocking the protein’s post-translational lipid modification, promotes T-cell-mediated suppression of tumour growth in mice.

High-throughput nanoparticle synthesis combined with machine learning speeds up the exploration of structure–activity relationships for nanomedicines, as shown for spherical nucleic acids functioning as cancer-vaccine candidates.

Immunotherapies developed to treat cancer can be adapted to treat autoimmunity.

A nanomedicine encapsulating a docetaxel prodrug, and conjugated to an antibody specific for the receptor EphA2, provides enhanced antitumour activity in multiple tumour-xenografted mice, and has minimal toxicity in rats and dogs.

Nanosensors of the activity of the protease granzyme B, which release a cleaved fluorescence reporter that filters into urine, enable the early diagnosis of acute transplant rejection in mice.

An immunotoxin incorporating an anti-programmed-cell-death-protein-1 (PD-1) single-chain variable fragment selectively eliminates PD-1-expressing cells, and suppresses autoimmunity while preserving adaptive immunity in mouse models of autoimmune disease.

The physiological degradation of programmed-death ligand 1 is reduced by the palmitoylation of its intracellular domain, and this process can be inhibited to promote T-cell immunity against tumours.

A methodology combining high-throughput nanoparticle synthesis and machine learning can be used to efficiently explore structure–activity relationships for nanomedicines, as shown by spherical nucleic acids functioning as cancer-vaccine candidates.