HIV-specific antibodies that mediate antibody-dependent cellular cytotoxicity vary in their paths to achieve function but commonly rely on mutations in multiple regions, including framework regions, to reach full potency.

Cytotoxicity associated with APOL1 renal-risk variants occurs through its plasma-membrane localization, where aberrant channel activity drives a sustained sodium and calcium influx leading to cell swelling and eventually cell death.

An unbiased genetic screen in human cells shows that the molecular target of a natural product with promising anticancer activity is a membrane phospholipid.

Staphylococcus aureus switches from innocuous coloniser to invasive human pathogen, the bacterial population can accumulate pathoadaptive mutations that reduce bacterial toxicity whilst allowing persistence within infected cells, potentially leading to severe human infections.

CD56/NCAM, the prototypical marker of human natural killer cells, promotes lytic function towards susceptible target cells by signaling through protein tyrosine kinase 2 (Pyk2).

Atomic structures of hIAPP fibrillar segments, determined using the cryo electron microscopy method MicroED, reveal that strong, stable intermolecular interactions are important features of cytotoxic amyloid proteins.

Longitudinal transcriptomic analysis of unvaccinated patients reveals that early NK cell cytotoxicity activation distinguishes mild from severe COVID-19, supporting the relevance of concerted innate–adaptive immune responses against the virus.

Topoisomerase 2α DNA breaks induced by G-quadruplex ligands are associated with a topological stress resulting from a transcription-dependent mechanism and counteracted by DNA topoisomerase 1 and factors promoting transcription elongation.

Multiple lines of evidence demonstrate that a single N-glycan on one receptor influences the strength of a cytotoxic response elicited by natural killer cells following stimulation with an antibody-coated target.

Phosphorylation of the phosphatase SHP-1 by PKC-θ in natural killer (NK) cells induces SHP-1 inhibition, revealing a novel molecular pathway that sustains NK cell activation threshold.