title: The fiendish behavior of TNF can be counteracted by microRNA.
abstract: Tumor necrosis factor (TNF) is a fascinating anti‐tumoral cytokine, which plays a key role in orchestrating the fight of innate immunity against infection. Concomitantly, TNF is a major player of the inflammatory response, as illustrated by successful therapeutic strategies targeting TNF in patho logies such as Crohn's diseases, rheumatoid arthritis or psoriasis. In mice, TNF is able to induce tissue injuries and lethal shock. In this issue of EMBO Molecular Medicine, Puimège et al (2015) elegantly demonstrated that the lethal shock induced by TNF reflects high levels of its receptor TNFRI as seen in sensitive (Mus musculus), vs. resistant (Mus spretus) mice, where TNFR1 expression is low. They reported that this expression is under the control of a microRNA (miR‐511), which itself is induced by glucocorticoids.
authors.affiliation: Unit Cytokines & Inflammation, Institut Pasteur, Paris, France.
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Cavaillon
mesh_terms: D000818:Animals; D005938:Glucocorticoids / Q000378:metabolism*; D035683:MicroRNAs / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D005938:Glucocorticoids; D035683:MicroRNAs; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha