Seman M
Laboratoire d'immunodifférenciation, Institut Jacques-Monod, CNRS-Université Paris 7.
Rev Prat. 1994 Jan 1;44(1):32-5.
Immune tolerance reflects the absence of immune reactions to self-antigens (natural tolerance) or exogenous antigens, at least in experimental models (acquired tolerance). It results in part from central mechanisms leading to the elimination or deletion of auto-reactive B or T cell clones by apoptosis in primary lymphoid organs. In the periphery, this is reflected by more-or-less reversible states of anergy, which arise from a time or spatial discordance between the different signals required for lymphocyte activation, or from a network of interactions between lymphocytes leading to the production of antagonistic signals. The reversibility of anergy-inducing mechanisms, a deregulation of the production of certain cytokines, or incomplete clonal deletion mechanisms could explain the emergence of autoimmune diseases by a rupture of self-tolerance. As these mechanisms are not fully understood, clinical induction of tolerance by the use of nonspecific immunodepressive agents is not yet possible.
免疫耐受反映了至少在实验模型中（获得性耐受）对自身抗原（天然耐受）或外源性抗原缺乏免疫反应。它部分源于中枢机制，该机制通过初级淋巴器官中自身反应性B或T细胞克隆的凋亡导致其消除或缺失。在周围组织中，这表现为或多或少可逆的无反应状态，其源于淋巴细胞激活所需的不同信号之间的时间或空间不一致，或源于淋巴细胞之间相互作用网络导致产生拮抗信号。无反应诱导机制的可逆性、某些细胞因子产生的失调或不完全的克隆缺失机制可以解释自身耐受的破坏导致自身免疫性疾病的出现。由于这些机制尚未完全了解，使用非特异性免疫抑制剂进行临床耐受诱导目前尚不可能。
