Alés-Martínez J E, Cuende E, Gaur A, Scott D W
Centro de Biología Molecular, Universidad Autónoma de Madrid, Spain.
Semin Immunol. 1992 Jun;4(3):195-202.
B cell tolerance is described as the absence of a measurable antibody forming response to an antigenic challenge. The establishment of antigen-specific tolerance requires, by definition, engagement of the B cell antigen-specific receptor. However, only in some circumstances does this engagement lead to tolerance, while in others it produces B cell activation and secretion of immunoglobulins. Several mechanisms occur naturally in vivo abrogating the expression of deleterious autoantibodies and contributing to the state of self-tolerance. In this review, we will examine different ways in which B cell tolerance can be broken, focusing on evidence showing that activated-T cells and/or their lymphokines can prevent B cell clonal deletion and thus have a potential role in the pathogenesis of autoimmune diseases. This approach is based on the well-known association of several lymphokines, such as IL-1, IL-2, IL-4, IL-5, and type I interferons, with autoimmune phenomena in vivo.
B细胞耐受性被描述为对抗抗原刺激时缺乏可测量的抗体形成反应。根据定义，抗原特异性耐受性的建立需要B细胞抗原特异性受体的参与。然而，只有在某些情况下，这种参与才会导致耐受性，而在其他情况下则会产生B细胞活化和免疫球蛋白分泌。体内自然发生几种机制，消除有害自身抗体的表达并有助于自身耐受状态。在本综述中，我们将研究打破B细胞耐受性的不同方式，重点关注表明活化T细胞和/或其淋巴因子可阻止B细胞克隆清除从而在自身免疫性疾病发病机制中具有潜在作用的证据。这种方法基于几种淋巴因子（如白细胞介素-1、白细胞介素-2、白细胞介素-4、白细胞介素-5和I型干扰素）与体内自身免疫现象的众所周知的关联。
