◀ Back to IL10
IL10 — IL1RN
Text-mined interactions from Literome
Mühlberg et al., J Clin Endocrinol Metab 2000
(Graves Disease) :
Recent data have indicated that orbital fibroblasts ( OF ) can be stimulated to produce marked quantities of
interleukin-1 receptor antagonist ( IL-1RA ), a powerful
inhibitor of the proinflammatory activities of
interleukin-1 in the orbital tissues in Graves ' ophthalmopathy ( GO )
Axtelle et al., J Endotoxin Res 2001
(Sepsis) :
IC14 inhibited the release of TNF-alpha, IL-6, and
IL-10 and
delayed the release of sTNFR ( I ) and
IL-1ra
Verheyen et al., Immunol Invest 2001
:
Both endogenous and exogenous
IL-10 suppressed IL-1beta and induced
IL-1Ra , thus markedly decreased the amount of functional IL-1
Kovár et al., Parasitol Res 2002
:
ELISA ( protein level ) and RNAse protection assay ( mRNA level ) showed that SGE
enhanced interleukin (IL)-1alpha, IL-1beta,
IL-1Ra , IL-6, and IL-12p40 cytokines, whereas production of IL-2, IL-5,
IL-10 , and IL-13 was decreased
Carl et al., J Leukoc Biol 2004
:
The regulation of secretory
interleukin (IL)-1 receptor antagonist ( sIL-1Ra ) in
response to
IL-10 is unique
Cominelli et al., Gastroenterology 1992
(Colitis) :
Recombinant
interleukin-1 receptor antagonist blocks the proinflammatory activity of endogenous
interleukin-1 in rabbit immune colitis
Tamassia et al., Int Immunol 2008
(Sepsis...) :
Consistent with the presence of a fully functional IL-10R, modulation of LPS induced CXCL8, CCL4, tumour necrosis factor-alpha and
IL-1ra gene expression was also rapidly
induced by
IL-10 in septic, but not normal, neutrophils
Darragh et al., Biochem J 2010
(Inflammation) :
MSKs regulate
IL-1ra transcription via both
IL-10 dependent and -independent mechanisms in cells
Burger et al., J Clin Invest 1995
:
The inhibitory activity of human
interleukin-1 receptor antagonist is
enhanced by type II
interleukin-1 soluble receptor and hindered by type I interleukin-1 soluble receptor
Hart et al., Immunology 1995
(Arthritis) :
Because
IL-10 and IL-4 differentially
regulate TNF-alpha and
IL-1ra production by synovial fluid mononuclear cells, selective use of either IL-10 or IL-4 in the treatment of chronic inflammatory conditions will depend on whether TNF-alpha or IL-1, respectively, is established as primarily responsible for the maintenance of the chronic inflammatory condition
Cassatella et al., J Exp Med 1994
:
In addition, we show that the release of
IL-1ra from LPS stimulated PMN is markedly potentiated in the
presence of
IL-10 ( from two to threefold after 18 h of stimulation ) ... Moreover, we observed that this
upregulation of
IL-1ra production by
IL-10 in LPS stimulated PMN took place through IL-1ra mRNA stabilization ... That
IL-10 selectively
upregulates IL-1ra production in LPS activated PMN, while it inhibits the production of IL-1 beta, TNF, and IL-8 under the same conditions, suggests that IL-10 may be an important physiologic regulator of cytokine production from PMN, and emphasizes the potential role of IL-10 in inflammatory responses
Jenkins et al., Lymphokine Cytokine Res 1994
:
The
effects of
interleukin-10 on
interleukin-1 receptor antagonist and interleukin-1 beta production in human monocytes and neutrophils ...
IL-10 alone
induced IL-1ra mRNA production in monocytes with a low level of protein production
Marie et al., Cytokine 1996
:
When
IL-1ra production by PMN was
induced by tumour necrosis factor-alpha (TNF-alpha),
IL-10 and IL-4 both amplified its release and its presence as a cell associated form
Thomassen et al., Clin Immunol Immunopathol 1996
(Inflammation) :
Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor ( TNF)-alpha, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8) ] and
enhances production of
interleukin-1-receptor antagonist ( IL-1ra ) from endotoxin stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown ... In contrast,
IL-1ra was not stimulated by LPS and basal levels were not
affected by
IL-10
Puren et al., J Clin Invest 1998
:
IL-18 did not
induce antiinflammatory cytokines,
IL-1Ra , or IL-10, although IL-18 induction of TNFalpha was inhibited by
IL-10