Skip to main content
. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: J Immunol. 2010 Apr 1;184(7):3311–3319. doi: 10.4049/jimmunol.0903778

FIGURE 1.

FIGURE 1

Pro- and anti-inflammatory axis of IL-10 depends on translation regulation. Left, Inflammatory stimuli activate p38 MAPK that disengages ARE binding proteins and derepresses the translation of inflammatory proteins. In a global anti-inflammatory role, IL-10 negatively regulates this process by abrogating the activation by p38 MAPK. Right, Occupancy of the adenosine receptors by its ligands relieves the imposed translational repression of IL-10 mRNA and activates the synthesis of IL-10 protein (blue circles). As a proinflammatory molecule, IL-10 stimulates ferritin translation by removing the translational repressor (the iron response element-binding protein) from 5′ UTR. Overproduction of ferritin causes sequestration of available iron (rust-colored circles) for bone marrow, leading to the characteristic anemia of inflammation.