Journal
NATURE IMMUNOLOGY
Volume 18, Issue 8, Pages 861-869Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3772
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Funding
- VIB
- Fund for Scientific Research Flanders (FWO)
- Foundation Against Cancer
- Ghent University (Concerted Research Actions, GOA)
- FWO postdoctoral fellowship
- FWO research grant
- Cancer Research Irvington Postdoctoral Fellowship
- Prevent Cancer Foundation Board of Directors Award
- American Association for the Study of Liver Diseases (AASLD) Pinnacle Research Award
- NIH [AI043477, CA163798]
- Leukemia and Lymphoma Society SCOR [20132569]
- Alliance for Lupus Research [257214]
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A properly mounted immune response is indispensable for recognizing and eliminating danger arising from foreign invaders and tissue trauma. However, the 'inflammatory fire' kindled by the host response must be tightly controlled to prevent it from spreading and causing irreparable damage. Accordingly, acute inflammation is self-limiting and is normally attenuated after elimination of noxious stimuli, restoration of homeostasis and initiation of tissue repair. However, unresolved inflammation may lead to the development of chronic autoimmune and degenerative diseases and cancer. Here, we discuss the key molecular mechanisms that contribute to the self-limiting nature of inflammatory signaling, with emphasis on the negative regulation of the NF-kappa B pathway and the NLRP3 inflammasome. Understanding these negative regulatory mechanisms should facilitate the development of much-needed therapeutic strategies for treatment of inflammatory and autoimmune pathologies.
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