The Therapeutic Potential of Modifying Inflammasomes and NOD-Like Receptors

Inflammasomes in cancer: a double-edged sword

“…Different inflammasomes are named for the NLR present in the complex, such as the NLRP3-, NLRC4-, NLRP1-, or NLRP6-inflammasome. In addition to the NLR inflammasomes, absent in melanoma 2 (AIM2), one of the PYHIN family members, is the main component of the AIM2 inflammasome (Schroder and Tschopp, 2010;Di Virgilio, 2013).…”

“…Sensing of danger signals by NLRs or AIM2 leads to the oligomerization and activation of caspase-1. Caspase-1 activates pro-IL-1β or pro-IL-18 by proteolytic cleavage, which in turn promotes inflammation and regulates immune responses (Zitvogel et al, 2012;Di Virgilio, 2013). Caspase-1 activation can also induce pyroptosis, an inflammatory cell death that is accompanied by the release of IL-1β and IL-18 which elicits local inflammation (Miao et al, 2011).…”

The P2X7 Receptor Channel: Recent Developments and the Use of P2X7 Antagonists in Models of Disease

“…These include the activation of the caspase-1-containing inflammasome NLRP3 and the subsequent processing and release of proinflammatory interleukin-1 (IL-1) cytokines, as well as the formation of reactive oxygen and nitrogen species and the formation of phagolysosomes and subsequent killing of intracellular pathogens (see Hewinson and Mackenzie, 2007;Miller et al, 2011;Di Virgilio, 2013). Here we will review recent developments in established signaling pathways and novel signaling pathways associated with P2X7.…”

The inflammasome as a target for pain therapy

“…NLRP1, NLRP3, NLRC4, and AIM2), 150 up to eight inflammasome subtypes have so far been described. 43 Future investigations delineating the specific role of these other subtypes in modulating pain may also aid in developing targeted therapies. An additional exciting frontier may be to exploit apparent differences in inflammasome subtypes between diseases to achieve tissue specificity when designing pharmaceutical therapies.…”