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IL1B — NOD2
Text-mined interactions from Literome
Oh et al., Cell Immunol 2005
:
Human umbilical vascular endothelial cells ( HUVECs ) minimally expressed NOD2 gene, whereas stimulation of HUVEC with bacterial LPS,
IL-1beta , or TNF-alpha
resulted in significant up-regulation of
NOD2
Ferwerda et al., Eur J Immunol 2008
(Crohn Disease) :
Although it is known that NOD2 mediates cytokine responses to muramyl dipeptide ( MDP ), it is yet unclear whether NOD2 stimulation mediates only transcription of pro-IL-1beta mRNA, or whether
NOD2 is also
involved in the activation of caspase-1 and release of active
IL-1beta
Rietdijk et al., Curr Opin Pharmacol 2008
(Inflammation) :
The
NOD proteins mediate NF-kappaB activation, whereas Pyrin molecules such as NALP3
regulate IL-1beta and IL-18 production
Hsu et al., Proc Natl Acad Sci U S A 2008
(Anthrax...) :
Yet, the molecular mechanism by which
NOD2 can
stimulate IL-1beta secretion, and its biological significance were heretofore unknown
Wikén et al., J Clin Immunol 2009
(Sarcoidosis) :
Combined TLR2 and
NOD2 stimulation
induced a four-fold higher secretion of TNFalpha and a 13-fold higher secretion of
IL-1 beta in patients
Martin et al., Arthritis Rheum 2009
(Arthritis...) :
Furthermore, functional studies demonstrate that caspase 1-mediated release of
IL-1beta also
involves NOD-2
Shio et al., PLoS Pathog 2009
(Disease Models, Animal...) :
Using knockout mice, we showed that Hz-induced
IL-1beta and inflammation are
dependent on
NOD-like receptor containing pyrin domain 3 ( NLRP3 ), ASC and caspase-1, but not NLRC4 ( NLR containing CARD domain )
Imamura et al., J Immunol 2010
(Shock, Septic) :
Interestingly, the
NOD of human PYNOD was
sufficient to inhibit caspase-1 mediated
IL-1beta secretion, whereas its pyrin domain was sufficient to inhibit ASC mediated NF-kappaB activation and apoptosis and to reduce ASC 's ability to promote caspase-1 mediated IL-1beta production
Swain et al., J Biosci 2013
(Bacterial Infections) :
In response to both Gram positive and Gram negative bacterial infections,
NOD1 and NOD2 receptors signalling were activated and
IL-1 beta , IL-8 and IFN- gamma were
induced