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A novel pathway was discovered for cellular uptake of LPS through secretory protein secretoglobin3A2 and a receptor syndecan-1, causing activation of non-canonical inflammasome pathway leading to pyroptosis of cancer cells.

Cellular, genetic, and biochemical assays shows that the application of a specific type of currents in mouse tendons induces an inflammatory response that favors the regeneration of the tissue, being a treatment for chronic tendinopathy lesions.

A signal for inflammatory cell death is induced by the disruption of cellular metabolism.

A cryo-electron microscopy model of the active human apoptosome illuminates how this "wheel of death" binds the protease procaspase-9 to initiate programmed cell death.

HOIL-1 deficiency in mice results in a severe immunodeficiency that is effectively complemented by chronic infection with a murine gamma-herpesvirus.

Genetic analyses using a new oral infection mouse model demonstrate that cell death pathways protect against the gastrointestinal bacterial pathogen Shigella flexneri.

CFTR modulators have potent innate anti-inflammatory properties that can be measured in clinic, both ex vivo and in vitro, which can be used to predict treatment efficacy.

Mutated NLRP3 forms cryo-sensitive aggregates that induce inflammasome assembly distinct from the canonical NLRP3 inflammasome.

Genetic labeling of cells that survive executioner caspase activity in Drosophila reveals distinct patterns in different tissues.

Wounded epidermal keratinocytes emit a signal that activates a specialized T-cell in the skin, leading to an increase in hair follicle stem cell numbers that contributes to tissue repair.