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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