News & Comment

Gail Bishop describes a 1985 study by Antonio Lanzavecchia that changed our understanding of B cell–T cell interactions.

In this Essay, Gérard Eberl presents a model of immunity that is based on an equilibrium between four types of immune response. Alteration of the internal or microbial environment leads to immune disequilibrium and determines immune protection or pathology.

The uptake of apoptotic corpses generates a molecular memory in macrophages that boosts the innate immune response.

Mitochondrial remodelling instructs metabolic adaptations in T cells.

Contact hypersensitivity induces a memory NK cell response that requires the NLRP3 inflammasome in tissue-resident macrophages.

Gasdermins induce pyroptosis by forming pores in the cell membrane.

Non-canonical inflammasome activation by self-derived oxidized phospholipid promotes both IL-1β release and cell survival.

Memory CD4⁺T cells promote vascular permeability, allowing protective antiviral antibodies to access neuronal tissue.

The SOCS family member CIS is a crucial negative regulator of IL-15-induced signalling in NK cells.

Maternally derived commensal-specific IgG helps to limit mucosal T cell responses in neonates.

Mice lacking CARD9 have altered microbiota with impaired tryptophan metabolism and therefore increased susceptibility to colitis.

HOBIT and BLIMP1 identified as universal regulators of tissue residency in lymphocytes.

The innate immune receptor LILRA2 (leukocyte immunoglobulin-like receptor subfamily A member 2) senses microbially cleaved immunoglobulin.

The Fanconi anaemia DNA repair pathway also has cytoplasmic functions in selective autophagy that might contribute to an inflammatory pathology of Fanconi anaemia disease.

Exposing mice to a dirty environment helps to 'humanize' their immune system.

Steven Ziegler describes a 1986 study by Mossmannet al. that defined two subsets of T helper cells on the basis of their activities.

Asymmetric distribution of metabolic pathway components sustains differential CD8⁺T cell fates.

Cyclodextrin promotes atherosclerosis regression through oxysterol-mediated, LXR-dependent macrophage reprogramming.

Biological scaffolds create an immune microenvironment that is favourable for tissue regeneration.

Akiko Iwasaki describes a 1980 study by Halleret al. that revealed a limitation of using inbred mice to study antiviral responses.