Madhusudhanan Sukumar

TL;DR: It is indicated that augmenting glycolytic flux drives CD8+ T cells toward a terminally differentiated state, while its inhibition preserves the formation of long-lived memory CD8+, and the efficacy of T cell-based therapies against chronic infectious diseases and cancer.

TL;DR: This work perturbed genes in human melanoma cells to mimic loss-of-function mutations involved in resistance to these therapies, using a genome-scale CRISPR–Cas9 library that consisted of around 123,000 single-guide RNAs, and profiled genes whose loss in tumours impaired the effector function of CD8+ T cells.

TL;DR: An ionic checkpoint that blocks T cell function in tumours is uncovered and potential new strategies for cancer immunotherapy are identified, including boosting potassium efflux in tumour-specific T cells by overexpressing the potassium channel Kv1.3.

TL;DR: Th17 cells, despite displaying low expression of CD27 and other phenotypic markers of terminal differentiation, efficiently eradicated tumors and caused autoimmunity, were long lived, and maintained a core molecular signature resembling early memory CD8(+) cells with stem cell-like properties.

TL;DR: How cell metabolism influences T cell anti-tumor activity, the metabolic qualities of highly-functional T cells, and strategies to modulate metabolism for improving the immune response to tumors are discussed.