Thewissen Marielle, Stinissen Piet
Hasselt University, Biomedical Research Institute and Transnationale Universiteit Limburg, School of Life Sciences, Diepenbeek, Belgium.
Crit Rev Immunol. 2008;28(5):363-76. doi: 10.1615/critrevimmunol.v28.i5.10.
Complex autoimmune diseases are chronic conditions initiated by a loss of immunological tolerance to self-antigens. Despite many years of intense investigation, the etiopathogenic mechanisms initiating these chronic inflammatory conditions remain undefined. The relatively high prevalence and the clustering of multiple autoimmune diseases within individuals or within families suggest that rather common immune mechanisms may facilitate the development of autoimmune diseases. However, specific genetic or environmental factors seem to be necessary for triggering disease. Clearly, immune mechanisms, which are intended to protect from disease, fail or become dysregulatcd. In this review, we discuss the mechanisms of immune homeostasis, immune regulation, and immunosenescence. We focus on the merit, consequences, and/or shortcomings of these mechanisms and speculate on their possible involvement in autoimmune-disease development.
复杂自身免疫性疾病是由对自身抗原免疫耐受丧失引发的慢性疾病。尽管经过多年深入研究，引发这些慢性炎症性疾病的病因发病机制仍不明确。个体或家族中多种自身免疫性疾病相对较高的患病率和聚集性表明，相当常见的免疫机制可能促进自身免疫性疾病的发展。然而，特定的遗传或环境因素似乎是触发疾病所必需的。显然，旨在预防疾病的免疫机制出现故障或失调。在本综述中，我们讨论免疫稳态、免疫调节和免疫衰老的机制。我们关注这些机制的优点、后果和/或缺点，并推测它们可能参与自身免疫性疾病发展的情况。
