Malek Thomas R
Department of Microbiology and Immunology, University of Miami School of Medicine, 1638 N.W. 10th Avenue, Room 718A, McKnight Building, Miami, FL 33136, USA.
J Leukoc Biol. 2003 Dec;74(6):961-5. doi: 10.1189/jlb.0603272. Epub 2003 Sep 2.
Based primarily on vitro studies, interleukin (IL)-2 has been considered a key growth and death factor for antigen-activated T lymphocytes. IL-2 is also essential to maintain self-tolerance, as IL-2- and IL-2 receptor-deficient mice exhibit lethal autoimmunity. The intrinsic death-sensitizing activity of IL-2 was thought to be a key mediator for apoptosis of peripheral autoreactive T cells. However, recent in vivo studies strongly favor a model whereby IL-2 controls autoimmunity through the production of CD4+CD25+ T regulatory (Treg) cells. In this setting, IL-2 is essential for expansion of Treg cells within the thymus and in peripheral neonatal-immune tissue. Thus, from being considered the primary growth factor for antigen-activated T lymphocytes, these new findings redefine the pivotal role for IL-2 as the major inducer for the developmental production of suppressive Treg cells.
主要基于体外研究，白细胞介素（IL）-2被认为是抗原激活的T淋巴细胞的关键生长和死亡因子。IL-2对于维持自身耐受性也至关重要，因为IL-2和IL-2受体缺陷的小鼠表现出致命的自身免疫。IL-2的内在死亡敏感活性被认为是外周自身反应性T细胞凋亡的关键介质。然而，最近的体内研究强烈支持一种模型，即IL-2通过产生CD4 + CD25 + T调节（Treg）细胞来控制自身免疫。在这种情况下，IL-2对于胸腺内和外周新生儿免疫组织中Treg细胞的扩增至关重要。因此，从被认为是抗原激活的T淋巴细胞的主要生长因子，这些新发现重新定义了IL-2作为抑制性Treg细胞发育产生的主要诱导剂的关键作用。
