When cells are stressed by aging, infection or environmental damage, they can release fragments of their own DNA into the cell interior. This misplaced DNA acts like an alarm, triggering inflammation meant to protect the body. But when that response goes unchecked, it can fuel chronic inflammation linked to conditions such as arthritis, neurodegenerative disease and other age-related disorders. Understanding how the immune system senses and controls these danger signals is a growing priority for human health.
In a new study published in Communications Biology from the lab of Assistant Professor Reginald McNulty at the Charlie Dunlop School of Biological Sciences, researchers uncovered a previously unknown role for a little-understood immune protein called NLRP10. The team found that NLRP10 can directly recognize and chemically bind to damaged DNA released from mitochondria, the cell’s energy producers. According to the paper, NLRP10 engages this oxidized DNA through a specific chemical interaction and then separates from another major immune sensor, NLRP3, once inflammation begins.
In simple terms, the study suggests that NLRP10 may help regulate inflammation rather than just turning it on. By interacting with damaged DNA and modulating its partnership with NLRP3, NLRP10 could help prevent inflammatory signals from becoming excessive or long-lasting. This kind of built-in restraint is especially important because persistent inflammation is a hallmark of aging and many chronic diseases.
The findings open new possibilities for designing therapies that reduce harmful inflammation without shutting down the immune system’s protective functions. More broadly, they highlight the value of fundamental research in revealing how our cells maintain balance under stress. Continued support for this work could pave the way for healthier aging and better treatments for inflammatory disease.