Abstract
Inflammation: gone with translation.
Highlights
Inflammation is a beneficial response of our immune system that protects us against infection and tissue injury
It was thought that the negative regulatory loops that kick in early to counteract inflammation were mainly a result of changes in mRNA levels either through transcriptional activation of inhibitory proteins or posttranscriptional repression of proinflammatory molecules by RNAbinding proteins (RBP) or microRNAs
Neutrophils are the first cells that localise to sites of tissue injury or infection, it is macrophages that orchestrate the multiple components of the inflammatory response through their ability to sense microbial products such as lipopolysaccharides (LPS), which bind tolllike receptor 4 (TLR4)
Summary
Inflammation (derived from the Latin inflammo, which means ‘‘I set alight’’) is a beneficial response of our immune system that protects us against infection and tissue injury. It was thought that the negative regulatory loops that kick in early to counteract inflammation were mainly a result of changes in mRNA levels either through transcriptional activation of inhibitory proteins or posttranscriptional repression of proinflammatory molecules by RNAbinding proteins (RBP) or microRNAs. A paper by Georg Stoecklin and colleagues at the German Cancer Research Center challenges this notion by demonstrating that, in the early stages of macrophage activation, translational derepression is a major mechanism that induces feedback inhibitors to dampen inflammation [1].
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