A Fellow of St Catharine’s had led international research that revealed shared traits across the immune systems of patients with unexplained autoinflammation, when the body’s immune system causes infl...

Pancreatic β-cell dysfunction and mass loss are core pathologies of type 2 diabetes mellitus (T2DM), which are closely related to intense autoinflammation. However, the molecular mechanisms regulating β-cell autoinflammation remain unclear. Here, we show that STING is significantly elevated in T2DM β cells. We also clarify the key role of uncoupling protein 2 (UCP2), and reveal that interleukin-1β (IL-1β) drives β cells to produce autoinflammation through the UCP2/mtDNA/STING axis in T2DM. To inhibit UCP2 activity in vivo, we design a tailored nanomedicine, Mito-G, with sequential targeting from islets to β-cell mitochondria. Mito-G is a negatively charged ultra-small nanomedicine synthesized by polymerization of genipin (a potent UCP2 inhibitor) and glycine. It can specifically reach β cells and have a natural mitochondrial targeting. In this work, Mito-G effectively eliminates β-cell auto-inflammation by specifically inhibiting β-cell UCP2 activity in vivo, providing a paradigm for t

Nature Communications - The relationship between pancreatic β-cell dysfunction and autoinflammation in T2DM is unclear. Here, the authors show the key role of a UCP2/mtDNA/STING axis in the...

The mechanisms linking defective protein prenylation to systemic inflammation in mevalonate kinase deficiency remain unclear. Munoz et al. reveal that mice and humans with MKD have defective NK cells,...

N-glycans on glycoRNAs prevent innate immune sensing of endogenous small RNAs, and the natural mechanism they use demonstrates how glycoRNAs exist on the cell surface and in the endosomal network with...

Autoinflammation of unknown origin remains amongst the most enigmatic of systemic autoinflammatory d

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Y-RNA activates RIG-I gain-of-function mutants in the kidney, causing lethal autoimmune diseases including lupus nephritis.