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Towards prevention of autoimmune diseases: The example of rheumatoid arthritis
European Journal of Immunology ( IF 4.5 ) Pub Date : 2021-06-10 , DOI: 10.1002/eji.202048952
Aase Hensvold 1, 2 , Lars Klareskog 1, 2, 3
Affiliation  

Prevention is the ultimate aim for clinicians and scientists concerned with severe diseases, like many immune-mediated conditions. Here, we describe recent progress in the understanding of etiology and molecular pathogenesis of rheumatoid arthritis (RA), which make this disease a potential prototype for prevention that may include both public health measures and targeted and personalized approaches that we call “personalized prevention.” Critical components of this knowledge are (i) better understanding of the dynamics of the RA-associated autoimmunity that may begin many years before onset of joint inflammation; (ii) insights into how this immunity may be triggered at mucosal surfaces after distinct environmental challenges; (iii) better understanding of which features of the pre-existing immunity may cause symptoms that precede joint inflammation and predict a high risk for imminent arthritis development; and (iv) how molecular events occurring before onset of inflammation might be targeted by existing or future therapies, ultimately by specific targeting of Major histocompatibility complex (MHC) class II restricted and RA-specific immunity. Our main conclusion is that studies and interventions in the phase of autoimmunity preceding RA offer new opportunities to prevent the disease and thereby also understand the molecular pathogenesis of its different variants.

中文翻译:

预防自身免疫性疾病:以类风湿性关节炎为例

预防是关注严重疾病(如许多免疫介导的疾病)的临床医生和科学家的最终目标。在这里,我们描述了对类风湿性关节炎 (RA) 病因学和分子发病机制的理解的最新进展,这使得这种疾病成为预防的潜在原型,可能包括公共卫生措施和我们称之为“个性化预防”的有针对性和个性化的方法。这些知识的关键组成部分是 (i) 更好地了解 RA 相关自身免疫的动态,这可能在关节炎症发作前多年开始;(ii) 深入了解在不同的环境挑战后如何在粘膜表面触发这种免疫;(iii) 更好地了解预先存在的免疫力的哪些特征可能导致关节炎症之前的症状并预测即将发生关节炎的高风险;(iv) 在炎症发生之前发生的分子事件如何被现有或未来的疗法靶向,最终通过特异性靶向主要组织相容性复合体 (MHC) II 类限制性免疫和 RA 特异性免疫。我们的主要结论是,RA 前自身免疫阶段的研究和干预为预防该疾病提供了新的机会,从而也了解了其不同变体的分子发病机制。最终通过特异性靶向主要组织相容性复合体 (MHC) II 类限制性免疫和 RA 特异性免疫。我们的主要结论是,RA 前自身免疫阶段的研究和干预为预防该疾病提供了新的机会,从而也了解了其不同变体的分子发病机制。最终通过特异性靶向主要组织相容性复合体 (MHC) II 类限制性免疫和 RA 特异性免疫。我们的主要结论是,RA 前自身免疫阶段的研究和干预为预防该疾病提供了新的机会,从而也了解了其不同变体的分子发病机制。
更新日期:2021-08-05
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