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Translation control: a multifaceted regulator of inflammatory response Mazumder B; Li X; Barik SJ Immunol 2010[Apr]; 184 (7): 3311-9A robust innate immune response is essential to the protection of all vertebrates from infection, but it often comes with the price tag of acute inflammation. If unchecked, a runaway inflammatory response can cause significant tissue damage, resulting in myriad disorders, such as dermatitis, toxic shock, cardiovascular disease, acute pelvic and arthritic inflammatory diseases, and various infections. To prevent such pathologies, cells have evolved mechanisms to rapidly and specifically shut off these beneficial inflammatory activities before they become detrimental. Our review of recent literature, including our own work, reveals that the most dominant and common mechanism is translational silencing, in which specific regulatory proteins or complexes are recruited to cis-acting RNA structures in the untranslated regions of single or multiple mRNAs that code for the inflammatory protein(s). Enhancement of the silencing function may constitute a novel pharmacological approach to prevent immunity-related inflammation.|Animals[MESH]|Gene Expression[MESH]|Gene Expression Regulation/*immunology[MESH]|Humans[MESH]|Inflammation/*genetics/*immunology[MESH]|Protein Biosynthesis/*immunology[MESH] |
