Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Despite major advances toward an improved understanding of the mechanisms leading to tumor immunity, the successful translation of mechanistic insights into effective tumor immunotherapy is hindered by a number of immunological obstacles. These include the ability of tumors to foster a tolerant microenvironment and the activation of a plethora of immunosuppressive mechanisms, which may act in concert to counteract effective immune responses. Here we will discuss different strategies employed by tumors to thwart immune responses, including tumor-induced impairment of antigen presentation, activation of negative costimulatory signals and elaboration of immunosuppressive and pro-apopoptic factors. In addition, we will underscore the influence of regulatory cell populations that may contribute to this immunosuppressive network including regulatory T cells, NKT cells and distinct subsets of immature and mature dendritic cells. The current wealth of preclinical information promises a future scenario in which the synchronized blockade of immunosuppressive mechanisms and the removal of inhibitory signals might be effective in combination with other conventional strategies to overcome immunological tolerance and promote tumor regression.