PGD₂ released after NAIP-NLRC4 inflammasome activation in tuft cells signals onto ILC3s and mediates host defense mechanisms against Salmonella Typhimurium within the small intestine. Tuft cells therefore not only promote immune reactions against parasites, but also bacteria.

This work demonstrates that group 2 KLF family transcription factors are critical for specifying the identity of distinct tissue-resident macrophages. KLF2 directly controls expression of genes previously shown to be necessary in cavity macrophages, while KLF4 may play a similar role in alveolar macrophages.

Jang et al. report that when the activating Kras mutation arises in hematopoietic stem cells, it causes the expansion and reprogramming of multipotent progenitors. These hypercompetitive progenitors lack self-renewal but rapidly spread the mutation throughout the blood system.

Broomfield et al. demonstrate that early type I interferon blockade alters CXCR3 chemokine regulation and cell location to promote an antigen-dependent CD8⁺ T cell transition of precursor of exhausted T cells to stem cell–like memory CD8⁺ T cells for enhanced protection following viral infection and mRNA–lipid nanoparticle vaccination.

This study unveils a novel mechanism by which the metabolic enzyme PCK1 hinders cGAS-STING activation by competitively consuming GTP, consequently fostering tumor immune evasion.

Sex hormones and chromosomes work in tandem to impact immune responses, with estrogen influencing class-switched memory B cell frequency exclusively in individuals with an XX chromosomal background.

Homozygous ATRIP splice variants are identified in patients with microcephalic primordial dwarfism and immunodeficiency, highlighting ATRIP’s essential role in the replication stress response, chromosomal stability, and immune cell viability and proliferation, providing insights into the molecular basis of these complex conditions.