Project Details
Description
The immune system identifies self and non-self molecules through pattern recognition receptors (PRRs) that detect pathogen-associated molecular patterns (PAMPs). Detection of PAMPs triggers a type I interferon response to eliminate the infection. Errors in this process, often due to mutations in nucleic acid sensors, can cause chronic type I interferon responses, leading to autoimmune and autoinflammatory diseases. This CRE aims to understand how self nucleic acids cause such diseases, particularly rare inherited forms, and develop treatments using advanced models. The research focuses on RNA sensing pathways, diseases from faulty nucleic acid sensing, and developing therapeutics. Findings could enhance RNA therapeutics and vaccines by improving our understanding of nucleic acid sensors. Additionally, this work could offer insights into rare genetic disorders and conditions like lupus, ALS, and Parkinsons disease, ultimately aiming to enable more precise and effective therapies.
Status | Active |
---|---|
Effective start/end date | 1/11/24 → 30/10/29 |
Fingerprint
Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.