◀ Back to IL10

HMGB1 — IL10

Text-mined interactions from Literome

Taniguchi et al., Arthritis Rheum 2003 (Arthritis, Rheumatoid...) : SFMs expressed RAGE and released TNFalpha, interleukin-1beta (IL-1beta), and IL-6 upon stimulation with HMGB-1
El Gazzar et al., Inflamm Res 2007 (Inflammation) : LPS induced HMGB1 release at 8 h and reached a peak at 48 h. Significant ( p < 0.05 ) production of TNFalpha, IL-1beta, IL-10 , and TGF-beta1 was seen after 8 h
Kamau et al., J Gen Virol 2009 : HMGB1 regulated tumour necrosis factor alpha, interleukin (IL)-6 , IL-8 and alpha interferon secretion in DENV infected DCs
Lynch et al., Am J Nephrol 2010 : HMGB-1 has also been observed as an extracellular secreted protein in serum of patients with sepsis and has putative intracellular signalling effects regulating the production of interleukin-1 and tumour necrosis factor in a number of inflammatory conditions
Carbone et al., Clin Cancer Res 2012 (Cell Transformation, Neoplastic...) : HMGB1 and Nalp3 induce proinflammatory responses and lead to interleukin-1ß and TNF-a secretion and NF-?B activity, thereby promoting cell survival and tumor growth
Weng et al., Shock 2012 (Acute Disease...) : Honokiol significantly reduced the increases in serum tumor necrosis factor-a, interleukin 1, and nitric oxide levels 3 h and serum high-mobility group box 1 24 h after acute pancreatitis induction
Wild et al., Int Immunol 2012 : Furthermore, HMGB1 enhances IL-10 release and T ( reg ) suppressive capacity in a RAGE dependent manner ... Furthermore, HMGB1 enhances IL-10 release and T ( reg ) suppressive capacity in a RAGE dependent manner
Chen et al., Immunotherapy 2013 (Acute Lung Injury...) : UA markedly rescued lethality, improved survival time and lung pathological changes, inhibited TNF-a, IL-6, IL-1ß, HMGB1 and NO, and increased IL-10 expression ... UA markedly rescued lethality, improved survival time and lung pathological changes, inhibited TNF-a, IL-6, IL-1ß, HMGB1 and NO, and increased IL-10 expression
Hutchison et al., Glia 2013 : Knockdown of miR-181 enhanced LPS induced production of pro-inflammatory cytokines ( TNF-a, IL-6, IL-1ß, IL-8 ) and HMGB1 , while overexpression of miR-181 resulted in a significant increase in the expression of the anti-inflammatory cytokine IL-10