Cell Death, Nucleic acids and Immunity: Inflammation beyond the Grave.
Arthritis & rheumatology (Hoboken, N.J.)
Cells of the innate immune system are rigged with sensors that detect nucleic acids derived from microbes, especially viruses. It has become clear that these same sensors that respond to nucleic acids derived from damaged cells or defective intracellular processing are implicated in triggering diseases such as lupus and arthritis. The ways in which cells die and the concomitant presence of proteins and peptides that allow nucleic acids to re-enter cells profoundly influence innate immune responses. This review briefly discusses different types of programmed necrosis such as pyroptosis, necroptosis and NETosis and explains how nucleic acids can engage intracellular receptors and stimulate inflammation. Host protective mechanisms that include compartmentalization of receptors and nucleases as well as the consequences of nuclease deficiencies are explored. Finally, we discuss proximal and distal targets in the nucleic acid stimulation of inflammation that are amenable to therapy to attenuate innate immune activation and disease pathogenesis. This article is protected by copyright. All rights reserved.
- 1Department of Medicine and Immunology, University of Washington, Seattle, Washington, USA.
This article is protected by copyright. All rights reserved.
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||Last Modified: 2016-03-27