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Thymic output is a dynamic process, with high activity at birth punctuated by transient periods of involution during infection. Interferon-α (IFN-α) is a critical molecular mediator of pathogen-induced thymic involution, yet despite the importance of thymic involution, relatively little is known about the molecular integrators that establish sensitivity. Here we found that the microRNA network dependent on the endoribonuclease Dicer, and specifically microRNA miR-29a, was critical for diminishing the sensitivity of the thymic epithelium to simulated infection signals, protecting the thymus against inappropriate involution. In the absence of Dicer or the miR-29a cluster in the thymic epithelium, expression of the IFN-α receptor by the thymic epithelium was higher, which allowed suboptimal signals to trigger rapid loss of thymic cellularity.

Original publication

DOI

10.1038/ni.2193

Type

Journal article

Journal

Nat Immunol

Publication Date

18/12/2011

Volume

13

Pages

181 - 187

Keywords

Animals, Arthritis, DEAD-box RNA Helicases, Female, Forkhead Transcription Factors, Male, Mice, MicroRNAs, Receptor, Interferon alpha-beta, Ribonuclease III, Thymus Gland