Parker D C, Eynon E E
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655.
FASEB J. 1991 Oct;5(13):2777-84. doi: 10.1096/fasebj.5.13.1916102.
In acquired tolerance, previous exposure to antigen under certain conditions induces specific unresponsiveness instead of specific immunological memory. It has been studied as an approach to the mechanisms of self-tolerance that operate on immunocompetent T and B lymphocytes once they leave their sites of origin in the thymus and the bone marrow. Possible mechanisms involve induction of specific suppressor cells or inactivation of antigen-specific lymphocytes (clonal anergy) as a consequence of abortive antigen presentation, in which the antigen receptor is effectively engaged but certain poorly defined accessory signals the T lymphocytes require are lacking. We propose that small, resting B lymphocytes, which lack these accessory signals, are the inactivating antigen-presenting cells in acquired tolerance to proteins and to the class II transplantation antigens. B lymphocytes, which can use their antigen receptors to gather and process antigens that are present at very low concentrations, may play a role in self-tolerance. In addition, B lymphocytes and T lymphocytes rendered anergic by encounter with self antigens could persist as self-specific suppressor cells to block an autoimmune response of autoreactive clones that had escaped deletion or anergy.
在获得性耐受中，先前在某些条件下接触抗原会诱导特异性无反应性，而非特异性免疫记忆。它已被作为一种研究自身耐受机制的方法，这种机制作用于免疫活性T淋巴细胞和B淋巴细胞，一旦它们离开胸腺和骨髓中的起源部位。可能的机制包括诱导特异性抑制细胞，或由于抗原呈递失败导致抗原特异性淋巴细胞失活（克隆无能），其中抗原受体被有效激活，但T淋巴细胞所需的某些定义不清的辅助信号缺失。我们提出，缺乏这些辅助信号的静止小B淋巴细胞是对蛋白质和II类移植抗原获得性耐受中的失活抗原呈递细胞。B淋巴细胞可以利用其抗原受体收集和处理极低浓度存在的抗原，可能在自身耐受中发挥作用。此外，因接触自身抗原而变得无能的B淋巴细胞和T淋巴细胞可能作为自身特异性抑制细胞持续存在，以阻断已逃脱缺失或无能的自身反应性克隆的自身免疫反应。
