Redmond William L, Sherman Linda A
Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
Immunity. 2005 Mar;22(3):275-84. doi: 10.1016/j.immuni.2005.01.010.
Whereas high-avidity recognition of peptide-MHC complexes by developing T cells in the thymus results in deletion and promotes self-tolerance, such recognition by mature T cells in the periphery results in activation and clonal expansion. This dichotomy represents the basis of a dilemma that has stumped immunologists for many years, how are self-specific T cells tolerized in the periphery? There appear to be two important criteria used to achieve this goal. The first is that in the absence of inflammatory pathogens, tolerance is promoted when T cells recognize antigen presented by quiescent dendritic cells (DCs) expressing low levels of costimulatory molecules. A second critical factor that defines "self" and drives tolerance through deletion, anergy, or suppression is the persistence of antigen.
在胸腺中发育的T细胞对肽-MHC复合物的高亲和力识别会导致细胞缺失并促进自身耐受,而外周成熟T细胞的这种识别则会导致激活和克隆扩增。这种二分法是一个困扰免疫学家多年的难题的基础,即外周的自身特异性T细胞是如何实现耐受的?实现这一目标似乎有两个重要标准。第一个是,在没有炎症病原体的情况下,当T细胞识别由表达低水平共刺激分子的静止树突状细胞(DC)呈递的抗原时,会促进耐受。定义“自身”并通过缺失、无反应性或抑制来驱动耐受的第二个关键因素是抗原的持续存在。