Discovery of Protein Switch for Regulating Viral and Autoimmune Immune Responses Offers Therapeutic Potential
Scientists have uncovered a vital protein switch involving SLIRP that controls immune responses to viruses and autoimmune diseases, highlighting new therapeutic possibilities for immune regulation.
Researchers from KAIST and Florida State University have identified a critical molecular mechanism involving the protein SLIRP, which functions as an immune switch controlling how cells respond to mitochondrial double-stranded RNA (mt-dsRNA). This discovery sheds light on how immune responses are amplified during viral infections and autoimmune diseases, such as Sjögren's syndrome and systemic lupus erythematosus.
The study demonstrates that SLIRP enhances immune activation by regulating mt-dsRNA, which structurally mimics viral RNA, leading to an increase in interferon responses. Elevated levels of SLIRP and mt-dsRNA observed in autoimmune tissues suggest its role in disease progression. Conversely, suppressing SLIRP reduces immune overactivation, highlighting its potential as a therapeutic target.
In viral context, inhibiting SLIRP diminishes antiviral responses, while in autoimmune tissues, its suppression alleviates excessive immune activity. These findings reveal SLIRP's dual function as a regulator of immune responses in both infections and autoimmune conditions. Professor Kim emphasizes that targeting SLIRP could lead to innovative treatments that modulate immune responses more precisely, benefiting patients with a range of immune-related diseases.
This study advances our understanding of immune regulation and opens new avenues for developing therapies aimed at balancing the body's defense mechanisms without causing tissue damage.
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