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Curr Opin Immunol. 2014 Dec;31:121-6. doi: 10.1016/j.coi.2014.10.009. Epub 2014 Nov 4.

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

Author information

1
Department of Cell Biology and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL, USA.
2
Department of Cell Biology and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL, USA. Electronic address: gbarber@med.miami.edu.

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.

PMID:
25459004
DOI:
10.1016/j.coi.2014.10.009
[Indexed for MEDLINE]

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