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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