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For our immune system to function effectively it must be able to tell the difference between “self” and “non-self” molecules.

A key component of this innate defence system are sensor proteins, which monitor the cell for foreign genetic material – such as DNA or RNA from a virus. When these “non-self” nucleic acid molecules are detected in a cell, it initiates a tailored response to the virus and helps to clear the infection.

Whilst these responses protect us from pathogens, it is essential that the cell can also accurately identify and tolerate cell-derived “self” nucleic acids. We now understand that mutations in nucleic acid sensing pathways can result in inappropriate detection of “self” nucleic acids as a threat and cause significant human disease.

Diseases associated with aberrant nucleic acid sensing span a spectrum from rare inherited disorders, such as Aicardi-Goutières syndrome and systemic lupus erythematosus, through to sporadic and more common diseases such as rheumatoid arthritis and psoriasis. Currently available therapies do not adequately address patient needs, and new approaches to diagnose, treat and provide symptom relief are required.

Our Vision

This Centre of Research Excellence will focus on understanding how “self” nucleic acids can trigger common and rare inherited autoinflammatory diseases associated with mutations in nucleic acid sensing pathways. The knowledge gained of these nucleic acid sensing pathways will be crucial for the development of more selective and effective therapies for these conditions.