Recent study could have major implications for our understanding of disease processes for conditions such as autoimmunity, atherosclerosis and heart failure, potentially leading to better prevention and treatment.

‘The innate immune response can be activated by a family of proteins called Toll-like receptors (TLRs). TLR signaling is responsible for maintaining immune homeostasis, which is the process of keeping the immune system stable.’

What Yeh and his team found is that a key signaling protein known as TRAF6 is kept in check by an inhibitory protein called sNASP to prevent accidental firing of the innate immune response. Animal studies supported this discovery - mice with a mutation that caused sNASP proteins to bind to TRAF6 proteins all the time were more susceptible to septic infection.
Experiments are in progress to study how sNASP mutations would affect the development of atherosclerosis and heart failure.





Source-Eurekalert