Review

Cellular and Molecular Life Sciences

, Volume 68, Issue 5, pp 765-783

Inflammasomes: current understanding and open questions

  • Franz BauernfeindAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Andrea AblasserAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Eva BartokAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Sarah KimAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Jonathan Schmid-BurgkAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Taner CavlarAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn
  • , Veit HornungAffiliated withUnit for Clinical Biochemistry, Institute for Clinical Chemistry and Clinical Pharmacology, University Hospital, University of Bonn Email author 

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Abstract

The innate immune system relies on its capability to detect invading microbes, tissue damage, or stress via evolutionarily conserved receptors. The nucleotide-binding domain leucine-rich repeat (NLR)-containing family of pattern recognition receptors includes several proteins that drive inflammation in response to a wide variety of molecular patterns. In particular, the NLRs that participate in the formation of a molecular scaffold termed the “inflammasome” have been intensively studied in past years. Inflammasome activation by multiple types of tissue damage or by pathogen-associated signatures results in the autocatalytic cleavage of caspase-1 and ultimately leads to the processing and thus secretion of pro-inflammatory cytokines, most importantly interleukin (IL)-1β and IL-18. Here, we review the current knowledge of mechanisms leading to the activation of inflammasomes. In particular, we focus on the controversial molecular mechanisms that regulate NLRP3 signaling and highlight recent advancements in DNA sensing by the inflammasome receptor AIM2.

Keywords

NLR NLRP3 AIM2 Caspase-1 IL-1β AIM2