Inflammasome Activation of IL-1 Family Mediators in Response to Cutaneous Photodamage†

Distinct Licensing of IL-18 and IL-1β Secretion in Response to NLRP3 Inflammasome Activation

Inflammasome activation permits processing of interleukins (IL)-1β and 18 and elicits cell death (pyroptosis). Whether these responses are independently licensed or are "hard-wired" consequences of caspase-1 (casp1) activity has not been clear. Here, we show that that each of these responses is independently regulated following activation of NLRP3 inflammasomes by a "non-canonical" stimulus, th...

IL-1 and IL-1 Are Endogenous Mediators Linking Cell Injury to the Adaptive Alloimmune Response

Azithromycin inhibits IL-1 secretion and non-canonical inflammasome activation

Deregulation of inflammasome activation was recently identified to be involved in the pathogenesis of various inflammatory diseases. Although macrolide antibiotics display well described immunomodulatory properties, presumably involved in their clinical effects, their impact on inflammasome activation has not been investigated. We compared the influence of macrolides on cytokine induction in hu...

Immune complexes inhibit IL-1 secretion and inflammasome activation.

IgG immune complexes have been shown to modify immune responses driven by APCs in either a pro- or anti-inflammatory direction depending upon the context of stimulation. However, the ability of immune complexes to modulate the inflammasome-dependent innate immune response is unknown. In this study, we show that IgG immune complexes suppress IL-1α and IL-1β secretion through inhibition of inflam...

Altered expression of IL-10 family cytokines in CRMO result in enhanced inflammasome activation

Introduction Chronic recurrent multifocal osteomyelitis (CRMO) is the most severe presentation of the autoinflammatory bone disorder chronic nonbacterial osteomyelitis (CNO). The pathophysiology of CNO remains to be determined. We recently demonstrated reduced activation of mitogen-activated protein kinases ERK1 and 2 in monocytes from CRMO patients responsible for impaired activation of the tr...