The innate immune response mounts a defence when immune cells recognize general hallmarks of infection, such as lipopolysaccharide (LPS) molecules, which are present in many types of bacterium. However, the inappropriate unleashing of an innate immune response can lead to autoimmune disorders. Gaining a better understanding of how innate immune responses are regulated might lead to improvements in clinical treatments for such disorders.
Writing in Nature, Zhong
et al.1 report that DNA synthesis in organelles called mitochondria has a key role in triggering an innate immune response.
Mitochondria can regulate how immune cells respond to infection and tissue damage. For example, these organelles can produce pro- or anti-inflammatory signals by altering the levels of metabolites produced in the Krebs cycle
2,
3, or by changing the level of production of reactive oxygen species (ROS)
4,
5. More and more examples are being found of mitochondrial functions being repurposed in unexpected ways to contribute to inflammatory signalling
2–
5.
