Centenary Institute and AW Morrow Gastroenterology and Liver Centre, Royal Price Alfred Hospital, University of Sydney, Newtown, NSW 2042, Australia.
Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16735-40. doi: 10.1073/pnas.1112251108. Epub 2011 Sep 20.
Although most self-reactive T cells are eliminated in the thymus, mechanisms to inactivate or control T cells specific for extrathymic antigens are required and exist in the periphery. By investigating the site in which autoreactive T cells are tolerized, we identify a unique mechanism of peripheral deletion in which naïve autoreactive CD8 T cells are rapidly eliminated in the liver after intrahepatic activation. T cells actively invade hepatocytes, enter endosomal/lysosomal compartments, and are degraded. Blockade of this process leads to accumulation of autoreactive CD8 T cells in the liver and breach of tolerance, with the development of autoimmune hepatitis. Cell into cell invasion, or emperipolesis, is a long-observed phenomenon for which a physiological role has not been previously demonstrated. We propose that this "suicidal emperipolesis" is a unique mechanism of autoreactive T-cell deletion, a process critical for the maintenance of tolerance.
虽然大多数自身反应性 T 细胞在胸腺中被清除,但需要存在于外周组织中能够使针对胸腺外抗原的 T 细胞失活或受到控制的机制。通过研究自身反应性 T 细胞耐受的部位,我们发现了一种独特的外周组织消除机制,即幼稚的自身反应性 CD8 T 细胞在肝内激活后迅速在肝脏中被消除。T 细胞主动侵入肝细胞,进入内体/溶酶体区室,并被降解。阻断这一过程会导致肝脏中自身反应性 CD8 T 细胞的积累和耐受的破坏,从而引发自身免疫性肝炎。细胞-细胞侵入,或吞噬作用,是一种长期观察到的现象,但以前没有证明其具有生理作用。我们提出,这种“自杀性吞噬作用”是自身反应性 T 细胞消除的一种独特机制,是维持耐受所必需的。