Self-DNA, STING-dependent signaling and the origins of autoinflammatory disease.

Abstract

Self-DNA has long been considered a key cause of inflammatory and autoimmune disease, although the exact origin and general mechanisms of action have remained to be elucidated. Recently, new insight has been gained into our understanding of those innate immune pathways and sensors that are responsible for instigating self-DNA triggered autoinflammatory events in the cell. One such sensor referred to as STING (for stimulator of interferon genes) has been found to be seminal for controlling cytosolic-DNA induced cytokine production, and may be responsible for a wide variety of inflammatory diseases including systemic lupus erythematosus (SLE), Aicardi-Goutieres syndrome (AGS) and STING-associated vasculopathy with onset of infancy (SAVI). STING may also be involved with augmenting certain types of carcinogen induced cancer. Aside from generating valuable information into mechanisms underlining innate immune gene regulation, these findings offer new opportunities to generate innovative therapeutics which may help treat such diseases.

• Authors: Jeonghyun Ahn, Glen N Barber
• Journal: Current opinion in immunology (Curr Opin Immunol) Vol. 31 Pg. 121-6 (Dec 2014) ISSN: 1879-0372 [Electronic] England
• PMID: 25459004 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2014 Elsevier Ltd. All rights reserved.

Chemical References

• Cytokines
• Membrane Proteins
• Neoplasm Proteins
• STING1 protein, human
• DNA

Topics

• Animals
• Autoimmune Diseases (immunology, pathology)
• Cytokines (immunology)
• DNA (immunology)
• Humans
• Inflammation (immunology, pathology)
• Membrane Proteins (immunology)
• Neoplasm Proteins (immunology)
• Neoplasms (immunology)
• Signal Transduction (immunology)