Gruber et al. identify STAT2 mutations in a family with severe early-onset pulmonary alveolar proteinosis (PAP), a rare lung disease marked by alveolar surfactant accumulation. By demonstrating that the excessive type I interferon inflammation driven by these STAT2 variants impairs monocyte chemotaxis, this study uncovers a novel mechanism of PAP.

In this work, we identify a new type I IFN–dependent psoriasis subtype resulting from rare heterozygous variants in ADAR1 and associated with a specific response to JAK1 and TYK2 inhibitors, opening new avenues in precision medicine in psoriatic disease.

We report four rare or common hypomorphic IL23R variants that, when present in the homozygous state, impair IFN-γ production by innate-like T and NK cells, thereby conferring a predisposition to tuberculosis.

Due to alternative splicing that removes the transmembrane domain–encoding exon, CD137 exists in both soluble and membrane forms. This study indicates that both forms of CD137 expressed by Foxp3⁺ CD4 T cells are critical for immunoregulation, and they independently restrain T1D development.

Alcaraz-Serna et al. have engineered regulatory T cells to specifically target the major birch pollen allergen Bet v1. These cells suppressed allergic immune responses and reduced airway inflammation in mice, opening novel strategic avenues for treating allergic asthma.

Yan et al. show that basal skull bridging vein–associated ACE structures enable CSF flow from the SAS into the dura, whereas spinal meninges lack these gateways, defining compartmentalized clearance regulated by anatomical exit zones and parenchymal border macrophages.

This study identifies a new mechanism driving kidney fibrosis. Researchers reveal that IFN-λ, produced by renal tubular epithelial cells, directly activates renal fibroblasts to cause fibrogenesis. Blocking IFN-λ signaling can delay progression of renal fibrosis.