生物谷報(bào)道：最近，在英國(guó)劍橋大學(xué)和馬塞諸塞州劍橋大學(xué)獨(dú)立工作的科學(xué)家們意外發(fā)現(xiàn)了一個(gè)能作用于整個(gè)免疫系統(tǒng)的調(diào)節(jié)網(wǎng)絡(luò),。該調(diào)節(jié)網(wǎng)絡(luò)有可能為人們提供關(guān)于機(jī)體免疫防御的機(jī)制和一系列包括霍奇金氏病在內(nèi)的淋巴瘤的新線索。該網(wǎng)絡(luò)依靠的是遺傳元件小RNA,。RNA與DNA關(guān)系密切,，功能繁多；由于這些微片斷過(guò)短而無(wú)法構(gòu)成基因,，卻可以和長(zhǎng)得多的信使RNA相互作用,，信使RNA由DNA翻譯而來(lái)，并指導(dǎo)蛋白質(zhì)的合成,。近10年來(lái)發(fā)現(xiàn)的約500個(gè)小RNA中,，有一個(gè)名為miR-155的小RNA在活化的B細(xì)胞和淋巴瘤中具有更高的豐度。由英國(guó)的Allan Brandley和Martin Turner領(lǐng)導(dǎo)的,，和哈佛醫(yī)學(xué)院Klaus Pajewsky領(lǐng)導(dǎo)的兩大科學(xué)家團(tuán)隊(duì)建立了一個(gè)敲除產(chǎn)生小RNA基因的小鼠系,。他們的報(bào)道今天發(fā)表在《科學(xué)》雜志上。Bradley醫(yī)生的團(tuán)隊(duì)發(fā)現(xiàn),，經(jīng)過(guò)基因處理的小鼠對(duì)接種沒有反應(yīng),，無(wú)法產(chǎn)生免疫。沒有miR-155,，它們無(wú)法產(chǎn)生重要的細(xì)胞因子,，細(xì)胞因子是細(xì)胞和細(xì)胞間的信號(hào)蛋白，可以協(xié)調(diào)免疫系統(tǒng)各個(gè)部分,。Rajewsky醫(yī)生的團(tuán)隊(duì)發(fā)現(xiàn)沒有miR-155,，免疫系統(tǒng)就沒法正確選擇特異的產(chǎn)生抗體的細(xì)胞來(lái)攻擊侵入者。Rajewsky醫(yī)生說(shuō)miR-155參與免疫系統(tǒng)是“全新的發(fā)展”,，將“引起巨大反思”,。到目前為止，許多免疫學(xué)家都以為免疫系統(tǒng)是在轉(zhuǎn)錄水平進(jìn)行調(diào)控的,，轉(zhuǎn)錄因子是控制基因的總開關(guān),。 “這種觀點(diǎn)影響了一代人的思考，”英國(guó)劍橋Babraham學(xué)院的Turner 醫(yī)生說(shuō),。但是這項(xiàng)發(fā)現(xiàn)顯示了另一個(gè)重要的調(diào)控水平,。 “敲除小RNA會(huì)影響很多相互作用的不同細(xì)胞，”Turner醫(yī)生說(shuō),。關(guān)于mi-155的工作為了解免疫系統(tǒng)打開了一扇窗,，但是現(xiàn)在就讓免疫學(xué)家轉(zhuǎn)化成應(yīng)用成果還為時(shí)過(guò)早。
Fig. 1. Mice deficient for bic/miR-155 show increased lung airway remodeling (A to F) Histological examination of sections of lung bronchioles from control wild-type (A, C, and E) and bicm1/m1 mice (B, D, and F). Scale bar, 100 µm. (A and B) Haematoxylin and eosin stain; (C and D) Masson Trichrome stain; (E and F) Immunohistochemical staining for smooth muscle actin. Collagen layer (white arrows), lung myofibroblasts (black arrows), bronchioles (B), and blood vessels (V) are indicated. (G) Quantitation of peribronchiolar collagen thickness or (H) airways smooth muscle cell (ASM) mass in bicm1/m1 mice compared with that of wild-type mice. (G) P < 0.02 or (H) P < 0.0001, in comparison with wild-type group, Student's two-tailed t test. Open circles, control mice; filled triangles, bicm1/m1 mice. Notably, bicm1/m1 mice with increased collagen layer thickness also had increased ASM mass. (I) Total and differential cell counts in BAL from the indicated mice. Data are the mean + SE from seven bic-deficient mice and six control mice. **P < 0.01 in comparison with wild-type group, Student's two-tailed t test.
原文出處：
Science 27 April 2007 Vol 316, Issue 5824
Requirement of bic/microRNA-155 for Normal Immune Function
Antony Rodriguez, Elena Vigorito, Simon Clare, Madhuri V. Warren, Philippe Couttet, Dalya R. Soond, Stijn van Dongen, Russell J. Grocock, Partha P. Das, Eric A. Miska, David Vetrie, Klaus Okkenhaug, Anton J. Enright, Gordon Dougan, Martin Turner, and Allan Bradley
Science 27 April 2007: 608-611.
Deletion of a microRNA sequence in mice impairs their immunity, causing abnormal immune responses and cytokine production, as well as gut and lung inflammation.
Abstract »| Full Text »| PDF »| Supporting Online Material »|
作者簡(jiǎn)介：
The Bradley Lab Homepage
相關(guān)基因：
MIRN155
Official Symbol: MIRN155 and Name: microRNA 155 [Homo sapiens]
Chromosome: 21
GeneID: 406947
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