Researchers from MD Anderson Cancer Center confirmed that ubiquitin-specific proteases (USP25) regulate the TLR4-dependent innate immune response by deubiquitinating the adaptor protein TRAF3. This research will help to understand the pathogenesis of autoimmune diseases and promote the development of targeted therapies. Related papers were published in the journal Science Signaling on May 14. Leading this research is Professor Chen Dong of MD Anderson Cancer Center, one of the world's top academics in immunology. The team led by him has made important contributions in the discovery of important immune tolerance regulator molecules. In 2009, he was awarded the Young Immunologist Award for Outstanding Achievement by the American Society of Immunology. He has published more than 120 papers and monographs in world-class academic journals.
Toll-like receptors (TLRs), as an important type of pattern recognition receptors (PRRs), are mainly expressed on the surface of macrophages and dendritic cells (DCs), selectively Identify pathogen-associated molecular patterns (PAMPs) and form the first barrier of the body's immune system against pathogen invasion. However, studies have also shown that excessive activation of innate immune responses activated by TLR signaling can lead to inflammatory diseases and autoimmune system diseases. It is of great theoretical significance and application value to deeply study the regulation mechanism of TLR signal transduction.
In this article, the researchers identified USP25 as an important regulator of TLR signaling. After lipopolysaccharide (LPS) stimulated TLR4, USP25 was recruited to the TLR4 signaling complex and bound to adaptor proteins TRAF3 and TRAF6. USP25 specifically reversed the E3 ubiquitin ligase cIAP2-mediated TRAF3 Lys48 ligated ubiquitination modification.
The researchers confirmed that USP25 deficiency can promote the ubiquitination level of TRAF3, accelerate the degradation of TRAF3 after TLR4 activation, thereby promoting TLR4-induced activation of NF-B and MAPK signals, and inhibiting the activation of the transcription factor IRF3. The researchers found that USP25-deficient mice were more sensitive to LPS-induced septic shock than wild-type mice, which was associated with increased production of pro-inflammatory cytokines and decreased production of interferon-α. Therefore, the new research results show that by inhibiting the degradation of TRAF3 during TLR4 activation, USP25 plays an extremely important role in regulating the balance of innate immune responses.
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