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探索：小RNA網(wǎng)絡(luò)保護(hù)胸腺免于不恰當(dāng)?shù)奈s
點(diǎn)擊次數(shù)：689 發(fā)布時(shí)間：2013-6-14
胸腺是T細(xì)胞發(fā)育的專門(mén)器官，它會(huì)隨著年齡的增長(zhǎng)出現(xiàn)循序漸進(jìn)的萎縮，病菌感染也會(huì)導(dǎo)致它出現(xiàn)周期性和可逆轉(zhuǎn)的萎縮，這個(gè)過(guò)程被稱為胸腺退化。年齡驅(qū)動(dòng)的退化可通過(guò)胸腺上皮細(xì)胞對(duì)性激素的敏感度來(lái)調(diào)節(jié)，感染引發(fā)的退化則可通過(guò)這些細(xì)胞對(duì)干擾素的敏感度來(lái)調(diào)控，α干擾素是一種免疫反應(yīng)的分子調(diào)控器。Adrian Liston和同事指出，小RNAs也就是調(diào)控蛋白質(zhì)產(chǎn)出的非編碼小RNAs，降低了胸腺上皮細(xì)胞對(duì)α干擾素信號(hào)的敏感度，因此，在保護(hù)胸腺免受感染引發(fā)的退化中發(fā)揮了關(guān)鍵作用。
The thymic epithelial microRNA network elevates the threshold for infection-associated thymic involution via miR-29a mediated suppression of the IFN-α receptor
Aikaterini S Papadopoulou, James Dooley, Michelle A Linterman, Wim Pierson, Olga Ucar, Bruno Kyewski, Saulius Zuklys, Georg A Hollander, Patrick Matthys, Daniel H D Gray, Bart De Strooper & Adrian Liston
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.