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Importantly, IpaB bound to its chaperone IpgC, as well as IpgC alone, did not cause IL-1 β secretion.
More recently, surface contact between macrophages and MSU crystals was shown to be sufficient to cause IL-1 β secretion in vitro via the NLRP3 inflammasome.
One of the important questions about IL-17 is the nature of the stimuli that cause IL-17 to be produced.
However, more recently, it was suggested that DAMPs, including microcrystals, are able to directly stimulate the release of endogenous ATP to cause IL-1β production in a P2X7-dependent mechanism (Riteau et al., 2012).
This has been effective at expanding NK cells but can cause IL-2 dependence of NK cells as well as toxicity in patients when the cytokine is given at high doses [ 49].
Although many agents cause IL-6 to be secreted, the overexpression or hypersecretion of IL-6 can be induced by arsenic exposure both in vivo (Das et al. 2005) and in vitro (Lee et al. 2005).
In addition to causing IL-1β secretion, α-hemolysin is known to induce cell death in numerous cell types [22].
As shown in Figures 7a and b, P2X7R stimulation caused IL-1 β release.
Increasing the severity of the injury caused IL-6 levels to more than double 1 day after injury.
We observed that co-culture of FLSs with CD4+ T cells resulted in production of IL-17, which caused IL-32 expression in FLSs.
Perturbation of tissue homeostasis causes IL-6 release in almost all situations and such a key cytokine is involved in surgical stress response as well.
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