Inflammation: gone with translation

Date

2014-06-19

Authors

Vinuesa, Carola
Preiss, Thomas

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Publisher

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.

Description

Keywords

cytokines, humans, inflammation, macrophage activation, macrophages, rna, messenger, signal transduction, toll-like receptor 4

Citation

Source

PLoS Genetics

Type

Journal article

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