Azevedo Pedro Correia, Murphy Grainne, Isenberg David A
Internal Medicine Department, Hospital Garcia de Orta, EPE, Almada, Portugal.
Methods Mol Biol. 2014;1134:1-16. doi: 10.1007/978-1-4939-0326-9_1.
Many studies have explored the pathology of systemic lupus erythematosus (SLE), an autoimmune rheumatic disorder with a striking female predominance. Numerous autoimmune phenomena are present in this disease, which ultimately result in organ damage. However, the specific cellular and humoral mechanisms underlying the immune dysfunction are not yet fully understood. It is postulated that autoimmunity is based on the interaction of genetic predisposition, hormonal and environmental triggers that result in reduced tolerance to self-tissues. These phenomena could occur because of altered antigen presentation, abnormalities in B cell responses, increases in the function of T-helper cells, abnormal cytokine production, exaggerated effector responses, or loss of regulatory T cells or B cells. Abnormalities in all of these components of the immune response have been implicated to varying degrees in the pathogenesis of SLE. This chapter will attempt to provide a "state-of-the-art" review of the evidence about the mechanisms underlying the pathology of SLE.
许多研究探讨了系统性红斑狼疮（SLE）的病理学，这是一种自身免疫性风湿性疾病，女性发病率显著偏高。该疾病存在多种自身免疫现象，最终会导致器官损伤。然而，免疫功能障碍背后具体的细胞和体液机制尚未完全明确。据推测，自身免疫基于遗传易感性、激素和环境触发因素之间的相互作用，这些因素会导致对自身组织的耐受性降低。这些现象可能是由于抗原呈递改变、B细胞反应异常、辅助性T细胞功能增强、细胞因子产生异常、效应反应过度或调节性T细胞或B细胞缺失所致。免疫反应的所有这些组成部分的异常在SLE发病机制中都不同程度地有所涉及。本章将试图对有关SLE病理学潜在机制的证据进行“最新”综述。
