人體神經(jīng)組織擁有一層嚴(yán)密的保護(hù)膜，但是一些免疫細(xì)胞仍能穿透保護(hù)膜進(jìn)入神經(jīng)系統(tǒng),，有時還會因此引發(fā)疾病,。德國科研人員日前報告說，他們利用新技術(shù)拍攝到免疫細(xì)胞入侵神經(jīng)系統(tǒng)的全過程,。
德國馬克斯·普朗克神經(jīng)生物學(xué)研究所等機(jī)構(gòu)的科研人員在英國《自然》雜志網(wǎng)站上報告說,，他們用綠色熒光蛋白為一種免疫細(xì)胞——T細(xì)胞打上標(biāo)記，將其放進(jìn)實驗鼠的血管內(nèi),，爾后利用“雙光子成像”技術(shù),，跟蹤被標(biāo)記細(xì)胞在實驗鼠機(jī)體內(nèi)的運動過程。
研究人員發(fā)現(xiàn),，T細(xì)胞入侵神經(jīng)系統(tǒng)的過程可分為幾個步驟：首先它會在血管中游動,，并且可以逆血流方向運動，檢查血管內(nèi)壁是否有異物,。然后它能穿過血管與神經(jīng)系統(tǒng)交界處的隔離膜,，并檢查血管外壁和神經(jīng)膜等組織。最后,，當(dāng)Ｔ細(xì)胞遇到一種吞噬細(xì)胞時,，就會發(fā)生不正常的免疫反應(yīng)，攻擊神經(jīng)系統(tǒng),，造成多發(fā)性硬化癥等疾病,。
“雙光子成像”技術(shù)即通過探測樣品經(jīng)雙光子激發(fā)后發(fā)出的熒光，實現(xiàn)樣品三維成像的技術(shù),。參與上述實驗的研究者說,，用該技術(shù)拍攝到生動直觀的Ｔ細(xì)胞活動影像,，不僅糾正了過去對這方面的一些錯誤認(rèn)識，而且大大增進(jìn)了對相關(guān)疾病發(fā)病原因的理解,，有助于研發(fā)針對多發(fā)性硬化癥等神經(jīng)系統(tǒng)疾病的治療手段,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature advance online publication 14 October 2009 | doi:10.1038/nature08478
Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions
Ingo Bartholom?us1,7, Naoto Kawakami1,7, Francesca Odoardi1,2,3, Christian Schl?ger1,2, Djordje Miljkovic1, Joachim W. Ellwart4, Wolfgang E. F. Klinkert1, Cassandra Flügel-Koch5, Thomas B. Issekutz6, Hartmut Wekerle1 & Alexander Flügel1,2,3
1 Max Planck Institute for Neurobiology, 82152 Martinsried, Germany
2 Department of Neuroimmunology, Institute for Multiple Sclerosis Research, Gemeinnützige Hertie-Stiftung and University Medical Centre G?ttingen, 37073 G?ttingen, Germany
3 Institute for Immunology, Ludwig-Maximilians-University, 80336 Munich, Germany
4 Institute for Experimental Hematology, Helmholtz Centre, 81377 Munich, Germany
5 Institute for Anatomy 2, Friedrich-Alexander-University, 91054 Erlangen, Germany
6 Division of Immunology, Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia B3K 6R8, Canada
7 These authors contributed equally to this work.
Correspondence to: Hartmut Wekerle1Alexander Flügel1,2,3 Correspondence and requests for materials should be addressed to A.F. or H.W.
The tissues of the central nervous system are effectively shielded from the blood circulation by specialized vessels that are impermeable not only to cells, but also to most macromolecules circulating in the blood. Despite this seemingly absolute seclusion, central nervous system tissues are subject to immune surveillance and are vulnerable to autoimmune attacks1. Using intravital two-photon imaging in a Lewis rat model of experimental autoimmune encephalomyelitis, here we present in real-time the interactive processes between effector T cells and cerebral structures from their first arrival to manifest autoimmune disease. We observed that incoming effector T cells successively scanned three planes. The T cells got arrested to leptomeningeal vessels and immediately monitored the luminal surface, crawling preferentially against the blood flow. After diapedesis, the cells continued their scan on the abluminal vascular surface and the underlying leptomeningeal (pial) membrane. There, the T cells encountered phagocytes that effectively present antigens, foreign as well as myelin proteins. These contacts stimulated the effector T cells to produce pro-inflammatory mediators, and provided a trigger to tissue invasion and the formation of inflammatory infiltrations.
