（視頻來源：MedPage Today）
來自美國拉赫拉過敏與免疫研究所的一組研究人員通過使用高科技成像技術，觀察到了小鼠胰腺內自身免疫性T淋巴細胞攻擊產生胰島素的胰島B細胞的過程，改發(fā)現(xiàn)在揭示I型糖尿病的發(fā)病機理中具有重大意義，其研究結果近日被發(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)病機理是感染(尤其是病毒感染)、毒物等因素誘發(fā)機體產生異常自身體液和細胞免疫應答,，導致胰島β細胞損傷,，胰島素分泌減少，多數(shù)患者體內可檢出抗胰島β細胞抗體,，通常需使用胰島素進行治療,。
研究人員發(fā)現(xiàn)，T細胞一開始在胰腺內漫無目的地隨機運動,，當其捕獲到胰島B細胞時,，便釋放毒性介質，數(shù)小時即可殺死胰島B細胞,。
研究者還發(fā)現(xiàn)了T細胞進入胰腺的特定血管,，人們或許可以通過該途徑阻止T細胞進入胰腺，從而達到治療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,，需要其體內數(shù)以千萬計的T淋巴細胞來破壞大量的胰島B細胞，這也解釋了I型糖尿病的臨床前期階段較長,。（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.
