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Red blood cells infected by the malaria parasite Plasmodium falciparum are destroyed by human natural killer cells in the presence of antibodies from people who have acquired clinical immunity to malaria.

By using structural methods to screen compounds for their ability to interact with amyloid beta, researchers have identified small molecules that stabilize amyloid fibers and reduce the toxic effect of smaller aggregates on cells.

Cytotoxic CD4 T lymphocytes are abundantly generated in T. cruzi-infected mice, predominantly infiltrate infected hearts, depend on T-cell intrinsic IL-18R/MyD88 signaling for expansion and their blood frequency correlates with the severity of chronic myocarditis in patients with Chagas disease.

L-mimosine and dopamine protect against cisplatin-induced oto- and nephrotoxicity in zebrafish and human cell line models.

Interleukin 15-producing microenvironments in the fetal and adult liver foster a type 1 innate lymphoid cell lineage with intrinsic cytotoxicity mediated through cytotoxic granules that are expressed under their steady state, unlike conventional natural killer cells with stimulation-dependent cytotoxicity.

Genetic engineering of murine myeloid cells reveals the challenges in ectopic expression of chemiric receptors and provides a novel framework to endow them with tumor-specific cytotoxic ability.

Rodent herpesvirus Peru overcomes NK ‘missing-self’ killing using a non-classical MHC-I like protein resistant todownregulation by its own ubiquitin ligase that potently sabotages antigen presentation to T-cells.

Cellular and genetic approaches reveal that exposure of a normally buried nuclear export signal (NES)-like sequence mediates export of ALS-linked mutant and misfolded wild-type SOD1 to the cytoplasm by CRM1.

The Shu complex enables lesion bypass of specific alkylation-induced DNA damage including abasic sites and 3-methyl-cytosine.