Diverse components of the tumor microenvironment affect T cell metabolism in ways that are crucial to improving immunotherapy.

Tregs form an "immunosuppressive ring" around solid tumors that is broken down during adoptive cell therapy and cyclophosphamide combination immunotherapy.

Tumor immunogenicity is quantified with a novel method, and the resulting tumor immunogenicity score is an effective tumor-inherent biomarker for prediction of response to immune checkpoint inhibitors.

Peptide immunotherapy in mice depends upon sustained expression of co-inhibitory protein PD-1 in T cells.

SLAMF6 is an inhibitory checkpoint of T cells, the lack of which leads to better tumor control, suggesting a new immunotherapy target.

Engineered T cell receptors enable targeted immunotherapy with a reduced risk of harmful autoimmunity.

Building on previous work (Lasagna-Reeves et al., 2015) it is shown that polyglutamine ATXN1 oligomers propagate locally in SCA1 mice, and that passive immunotherapy targeting soluble oligomers can lead to an improvement in motor coordination and a modest increase in life span.

Immune checkpoint inhibition therapy for cancer paradoxically activates tuberculosis infection, and advanced human cell culture modelling demonstrates excess TNF-α section is the primary driver.

Why does cancer develop in situations where the immune system is perfectly capable of eliminating it?

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.