Inflammation: gone with translation
Date
2014-06-19
Authors
Vinuesa, Carola
Preiss, Thomas
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Public Library of Science
Abstract
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. Like all immune responses, it needs
to be tightly controlled: excessive inflammatory
responses can lead to both acute
diseases, such as septic shock, and chronic
diseases, such as rheumatoid arthritis,
atherosclerosis, and cancer. Until recently,
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
now 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.
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Keywords
cytokines, humans, inflammation, macrophage activation, macrophages, rna, messenger, signal transduction, toll-like receptor 4
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PLoS Genetics
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Journal article
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