（視頻來(lái)源：MedPage Today）
來(lái)自美國(guó)拉赫拉過(guò)敏與免疫研究所的一組研究人員通過(guò)使用高科技成像技術(shù)，觀察到了小鼠胰腺內(nèi)自身免疫性T淋巴細(xì)胞攻擊產(chǎn)生胰島素的胰島B細(xì)胞的過(guò)程，改發(fā)現(xiàn)在揭示I型糖尿病的發(fā)病機(jī)理中具有重大意義，其研究結(jié)果近日被發(fā)表在《臨床研究雜志》（Journal of Clinical Investigation）上。
I型糖尿病是一種自身免疫性疾病,，又稱胰島素依賴性糖尿病，發(fā)病人群年齡較小，其發(fā)病機(jī)理是感染(尤其是病毒感染),、毒物等因素誘發(fā)機(jī)體產(chǎn)生異常自身體液和細(xì)胞免疫應(yīng)答，導(dǎo)致胰島β細(xì)胞損傷,，胰島素分泌減少,，多數(shù)患者體內(nèi)可檢出抗胰島β細(xì)胞抗體，通常需使用胰島素進(jìn)行治療,。
研究人員發(fā)現(xiàn),，T細(xì)胞一開(kāi)始在胰腺內(nèi)漫無(wú)目的地隨機(jī)運(yùn)動(dòng)，當(dāng)其捕獲到胰島B細(xì)胞時(shí),，便釋放毒性介質(zhì),，數(shù)小時(shí)即可殺死胰島B細(xì)胞。
研究者還發(fā)現(xiàn)了T細(xì)胞進(jìn)入胰腺的特定血管,，人們或許可以通過(guò)該途徑阻止T細(xì)胞進(jìn)入胰腺,，從而達(dá)到治療I型糖尿病的目的。
研究者指出,，要使小鼠發(fā)展成為I型糖尿病,，需要其體內(nèi)數(shù)以千萬(wàn)計(jì)的T淋巴細(xì)胞來(lái)破壞大量的胰島B細(xì)胞，這也解釋了I型糖尿病的臨床前期階段較長(zhǎng),。（生物谷bioon.com）
doi:10.1172/JCI59285
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Intravital imaging of CTLs killing islet cells in diabetic mice
Ken Coppieters, Natalie Amirian and Matthias von Herrath.
Type 1 diabetes (T1D) is caused by autoimmune destruction of the insulin-producing β cells in the pancreatic islets, which are essentially mini-organs embedded in exocrine tissue. CTLs are considered to have a predominant role in the autoimmune destruction underlying T1D. Visualization of CTL-mediated killing of β cells would provide new insight into the pathogenesis of T1D, but has been technically challenging to achieve. Here, we report our use of intravital 2-photon imaging in mice to visualize the dynamic behavior of a virally expanded, diabetogenic CTL population in the pancreas at cellular resolution. Following vascular arrest and extravasation, CTLs adopted a random motility pattern throughout the compact exocrine tissue and displayed unimpeded yet nonlinear migration between anatomically nearby islets. Upon antigen encounter within islets, a confined motility pattern was acquired that allowed the CTLs to scan the target cell surface. A minority of infiltrating CTLs subsequently arrested at the β cell junction, while duration of stable CTL–target cell contact was on the order of hours. Slow-rate killing occurred in the sustained local presence of substantial numbers of effector cells. Collectively, these data portray the kinetics of CTL homing to and between antigenic target sites as a stochastic process at the sub-organ level and argue against a dominant influence of chemotactic gradients.
