A new study led by immunobiology experts at Cincinnati Children’s has provided important insights into the mechanisms behind cytokine storms, a dangerous form of infection-triggered inflammation. Published in the journal Cell Reports, the study reveals how effector memory T cells (Tem) and dendritic cells interact to initiate a chain of reactions that lead to the release of cytokines, which can cause damage to cells and organs.
The team found that ongoing encounters between Tem cells and dendritic cells can lead to DNA damage within the dendritic cells, triggering a DNA repair pathway that generates large numbers of inflammatory cytokines. This cytokine storm is responsible for the tissue damage seen in conditions such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases.
The researchers also identified the role of the stimulator of interferon genes (STING) pathway in driving the production of cytokines. By disrupting the interaction between STING and TRAF6, a gene and transcription factor involved in inflammation, the researchers were able to prevent the production of innate cytokines in mice.
The findings have implications for the treatment of autoimmune diseases and cancer, as disrupting the inflammatory cascade at an early stage could help prevent the development of cytokine storms. However, further research is needed to confirm whether medications that target key points along this pathway can effectively control inflammation.
The study highlights the importance of understanding the complex interplay between different components of the immune system in order to develop targeted therapies for cytokine storms and other inflammatory diseases.
– Cell Reports journal article
– Cincinnati Children’s research team