Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
PLoS Biol. 2023 Apr 25;21(4):e3002084. doi: 10.1371/journal.pbio.3002084. eCollection 2023 Apr.
Systemic autoimmune diseases are characteristically associated with aberrant autoreactive innate and adaptive immune responses that lead to tissue damage and increased morbidity and mortality. Autoimmunity has been linked to alterations in the metabolic functions of immune cells (immunometabolism) and, more specifically, to mitochondrial dysfunction. Much has been written about immunometabolism in autoimmunity in general, so this Essay focuses on recent research into the role of mitochondrial dysfunction in the dysregulation of innate and adaptive immunity that is characteristic of systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Enhancing the understanding of mitochondrial dysregulation in autoimmunity will hopefully contribute to accelerating the development of immunomodulatory treatments for these challenging diseases.
系统性自身免疫性疾病的特征是与异常的自身反应性先天和适应性免疫反应相关，这些反应会导致组织损伤和发病率及死亡率增加。自身免疫与免疫细胞的代谢功能改变（免疫代谢）有关，更具体地说，与线粒体功能障碍有关。关于自身免疫中的免疫代谢已经有很多文献报道，因此本文重点介绍了最近关于线粒体功能障碍在系统性自身免疫性疾病（如系统性红斑狼疮（SLE）和类风湿关节炎（RA））中固有和适应性免疫失调中的作用的研究。深入了解自身免疫中的线粒体失调有望有助于加速为这些具有挑战性的疾病开发免疫调节治疗方法。
