Abstract |
Extensive research through the years has revealed that during an autoimmune disease, such as multiple sclerosis (MS), impaired T regulatory cell function could be responsible for the unbalanced tolerance against autoantigens, leading to disease susceptibility and affecting the course of autoimmunity. In parallel, studies have demonstrated that even though in the early stages of MS the pathology development is mainly controlled by inflammation, the progression of the disease is affected by mitochondrial impairment. In addition, It has been proved that disorders of mitochondrial dynamics can contribute to the pathogenesis of neurodegenerative diseases as well as in the pathogenesis of autoimmune diseases.
Even though impaired mitochondrial function is found to be implicated in autoimmunity and directly affects the cell growth and survival, the role of defective mitochondrial clearance by autophagy (mitophagy) in Treg cell function and survival, remains to be delineated.
In this context, aim of this study is to further assess the role of autophagy in Treg cells and shed light to the role of mitophagy in T regulatory mediated suppression during an autoimmune response, and more specifically in the context of multiple sclerosis. Understanding the implication of mitochondria clearance in autoimmunity could provide new evidence in MS pathogenesis, as well as in other autoimmune disorders, and lead to the discovery of new therapeutic targets.
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