Remyelination, the process by which axons are re-encased in myelin after injury, is a critical step in restoring brain function, yet the dynamics from initial injury to repair remain poorly characteri...

Kurt-Jones et al. examined IFN-ε, a hormone-responsive type I IFN expressed by genital epithelial cells, during Neisseria gonorrhoeae (Ng) infection. They demonstrated that mice lacking IFN-ε exhibit ...

Liu et al. illustrate a comprehensive transcriptomic landscape of NPC and CN TLSs, identifying an interferon-activated HEV subset (IFN-HEV) that secretes CXCL9 to drive TLS assembly. Leveraging features of IFN-HEVs, the CTRscore is developed and exhibits superior accuracy in predicting response to anti-PD-1 immunotherapy in NPC.

Recent insights reveal that type I interferon (IFN-I) signalling plays critical roles in the nervous system beyond antiviral defence. Dysregulated IFN-I activity is increasingly linked to neurologica...

Signal Transduction and Targeted Therapy - When vaccines reset tumors: SARS-CoV-2 mRNA shots create a transient checkpoint-sensitive state

STING–type-I interferon pathway regulates the immunogenicity of several cancer types, including head and neck squamous cell carcinoma. Here the authors describe that glutamine metabolism in the tumour...

Successful cancer immunotherapy is associated with high numbers of neutrophils and expression of IRF1.

Alzheimer’s disease (AD) disproportionately affects women, yet the biological basis of this sex bias remains unclear. Here, we identify sex-dependent interferon signaling as a contributor to this disparity. Transcriptomic profiling of postmortem AD tissue and APP/PS1 mice revealed preferential enrichment of interferon-responsive gene programs in females. In APP/PS1 mice, heightened interferon responses were associated with increased neurodegenerative features, and single-cell transcriptomic analyses identified microglia as a major cellular compartment engaging interferon responses. To test causality, we manipulated interferon signaling in vivo. Acute systemic interferon activation promoted AD-like neuropathological alterations. Genetic amplification of interferon signaling in microglia exacerbated neuroinflammatory and neurodegenerative features in APP/PS1 mice, whereas pharmacological inhibition through cGAS-STING blockade suppressed interferon responses, reduced neuropathology, and preserved cognitive performance in female APP/PS1 mice. Together, these findings identify microglial interferon signaling as a modifiable contributor to AD-associated neuropathology and suggest a neuroimmune mechanism underlying the increased vulnerability of females to the disease.

Stunnenberg et al. use a model of lipopolysaccharide injection in humans to characterize the transcriptomic landscape of bone marrow and blood immune cells during the hyperinflammatory and immunosuppr...

This study explores the use of ultrasound contrast agents loaded with Stimulator of Interferon Genes (STING) agonists as an approach to activate the body's immune system against cancer. Termed Microb...

Cytokine receptor dimerization, induced by the binding of cytokines, can be converted into a genetically traceable fluorescent signal and engineered into reporter mouse lines to visualize processes in vivo. An interleukin-17A reporter mouse line clarifies the location of IL-17A responsive cells in the ileum, while an interferon-γ line can highlight relevant effector populations of T cells in tumors.