Wen L, Wong F S
Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, Mailbox 208020, 333 Cedar Street, New Haven, CT 06520, USA.
Crit Rev Immunol. 2005;25(3):225-50. doi: 10.1615/critrevimmunol.v25.i3.40.
The environment is important in determining the onset of autoimmune diseases such as type 1 diabetes. Genetic susceptibility factors interact with the environment to trigger and modulate a series of immune responses that ultimately lead to destruction of the insulin-producing beta cells of the pancreas. Although T lymphocytes are thought to play a major pathogenic role in the pathogenesis of diabetes, undoubtedly other components of the immune system also contribute to this process. How the environment may alter the course of disease is unknown, although viruses have been implicated in triggering and/or exacerbating the disease process. In this review, we will focus on how infection, particularly with viruses, may influence the onset of type 1 diabetes and other autoimmune diseases. Mechanisms such as molecular mimicry, bystander activation, and uncontrolled polyclonal activation of the immune system may contribute to the immune pathogenesis. We will also explore the interaction of the innate immune system with adaptive immune responses in predisposing individuals to the development of autoimmunity.
环境在决定自身免疫性疾病(如1型糖尿病)的发病方面很重要。遗传易感因素与环境相互作用,触发并调节一系列免疫反应,最终导致胰腺中产生胰岛素的β细胞被破坏。虽然T淋巴细胞被认为在糖尿病发病机制中起主要致病作用,但毫无疑问,免疫系统的其他成分也参与了这一过程。尽管病毒被认为与触发和/或加剧疾病进程有关,但环境如何改变疾病进程尚不清楚。在这篇综述中,我们将重点关注感染,特别是病毒感染,如何影响1型糖尿病和其他自身免疫性疾病的发病。分子模拟、旁观者激活和免疫系统不受控制的多克隆激活等机制可能有助于免疫发病机制。我们还将探讨先天免疫系统与适应性免疫反应在使个体易患自身免疫性疾病方面的相互作用。