免疫系统的主要任务是保护免受传染性病原体的侵害，通过识别和抵消环境中的有害物质来维持自身稳态，以及监测病理性，例如肿瘤组织的变化。它通过天然免疫和适应性免疫系统的细胞和体液成分之间的复杂相互作用来完成这些任务。本综述文章重点讨论了B和T淋巴细胞在适应性免疫携带者中自我与非我识别的核心问题。在骨髓中淋巴细胞成熟期间，通过体细胞重组随机产生了大量的淋巴细胞受体库，其整体具有识别任何外来抗原的能力。为了降低可能由于进化保守的结构基序在自身和外来抗原中产生自身免疫攻击的内在风险，适应性免疫系统必须提供冗余机制（克隆删除，无反应，静止和抑制）来消除或失活表达高亲和力自身抗原受体的淋巴细胞。因此，通过感染，分子模仿，破坏的凋亡调节，通过后翻译修饰改变“自体”以及转录因子和信号组分的遗传变化等方式提供共刺激信号，可以降低潜在自身反应性的无反应性T细胞的激活门槛，从而导致自身耐受性的破坏和发病性自身免疫病的诱导。©2023年作者，独家授权给施普林格·梅迪欣出版社股份有限公司，施普林格·自然集团的一部分。

The major tasks of the immune system are protection against infectious agents, maintaining homeostasis by recognizing and neutralizing noxious substances from the environment, and monitoring pathological, e.g. neoplastic tissue changes. It accomplishes these tasks through complex interactions of cellular and humoral components of the innate and adaptive immune system. This review article focuses on a central problem of self versus non-self discrimination in the development of B and T lymphocytes as carriers of adaptive immunity. During maturation of the lymphocytes in the bone marrow, large repertoires of lymphocyte receptors are randomly generated by somatic recombination, which as a whole have the capability of recognizing any foreign antigen. In order to reduce the implicit risk of autoaggressive immunity that might arise from evolutionary conserved structural motifs in self and foreign antigens, the adaptive immune system must provide redundant mechanisms (clonal deletion, anergy, quiescence and suppression) to eliminate or inactivate lymphocytes expressing highly avid receptors for autoantigens. Thus, the provision of costimulatory signals resulting in a reduced activation threshold of potentially autoreactive anergic T cells through infection, molecular mimicry, disrupted apoptosis regulation, altered "self" by post-translational modification, genetic changes in transcription factors with critical importance for thymic tolerance induction or signaling components of apoptosis can lead to a disruption of self-tolerance and the induction of pathogenic autoimmunity.© 2023. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.