Broegelmann Research Laboratory, The Gade Institute, University of Bergen, Bergen, Norway.
Immunol Lett. 2011 Dec 30;141(1):1-9. doi: 10.1016/j.imlet.2011.06.007. Epub 2011 Jul 12.
In Sjögren's syndrome, like in most other autoimmune diseases, the enigma leading to a pathogenic attack against self has not yet been solved. By definition, the disease must be mediated by specific immune reactions against endogenous tissues to qualify as an autoimmune disease. In Sjögren's syndrome the autoimmune response is directed against the exocrine glands, which, as histopathological hallmark of the disease, display persistent and progressive focal mononuclear cell infiltrates. Clinically, the disease in most patients is manifested by two severe symptoms: dryness of the mouth (xerostomia) and the eyes (keratoconjunctivitis sicca). A number of systemic features have also been described and the presence of autoantibodies against the ubiquitously expressed ribonucleoprotein particles Ro (Sjögren's-syndrome-related antigen A - SSA) and La (SSB) further underline the systemic nature of Sjögren's syndrome. The original explanatory concept for the pathogenesis of Sjögren's syndrome proposed a specific, self-perpetuating, immune mediated loss of acinar and ductal cells as the principal cause of salivary gland hypofunction. Although straightforward and plausible, the hypothesis, however, falls short of accommodating several Sjögren's syndrome-related phenomena and experimental findings. Consequently, researchers considered immune-mediated salivary gland dysfunction prior to glandular destruction and atrophy as potential molecular mechanisms underlying the symptoms of dryness in Sjögren's syndrome. Accordingly, apoptosis, fibrosis and atrophy of the salivary glands would represent consequences of salivary gland hypofunction. The emergence of advanced bio-analytical platforms further enabled the identification of potential biomarkers with the intent to improve Sjögren's syndrome diagnosis, promote the development of prognostic tools for Sjögren's syndrome and the long-term goal to identify possible processes for therapeutic treatment interventions. In addition, such approaches allowed us to glimpse at the apparent complexity of Sjögren's syndrome.
在干燥综合征中,与大多数其他自身免疫性疾病一样,导致针对自身的致病性攻击的谜团尚未解决。根据定义,疾病必须由针对内源性组织的特定免疫反应介导,才能被视为自身免疫性疾病。在干燥综合征中,自身免疫反应针对的是外分泌腺,这些腺体作为疾病的组织病理学特征,显示出持续和进行性的局灶性单核细胞浸润。临床上,大多数患者的疾病表现为两种严重症状:口干(xerostomia)和眼睛干燥(keratoconjunctivitis sicca)。还描述了许多全身性特征,并且针对普遍表达的核糖核蛋白颗粒 Ro(干燥综合征相关抗原 A - SSA)和 La(SSB)的自身抗体的存在进一步强调了干燥综合征的全身性。最初提出的干燥综合征发病机制的解释概念认为,腺泡和导管细胞的特异性、自我延续的免疫介导丧失是唾液腺功能减退的主要原因。尽管该假说简单而合理,但它未能解释干燥综合征的几个相关现象和实验发现。因此,研究人员认为,免疫介导的唾液腺功能障碍先于腺体破坏和萎缩,是干燥综合征干燥症状的潜在分子机制。因此,唾液腺的细胞凋亡、纤维化和萎缩将代表唾液腺功能减退的后果。先进的生物分析平台的出现进一步使我们能够识别潜在的生物标志物,旨在改善干燥综合征的诊断,促进干燥综合征预后工具的开发,并长期目标是确定可能的治疗干预过程。此外,这些方法使我们能够一窥干燥综合征的明显复杂性。