Autophagy exerts its dual role in eukaryotic cells and exerts its cytoprotective action through degradation mechanism and by regulating catabolic processes which results in elimination of pathogens. Under suitable conditions, autophagy is associated with recycling of cytoplasmic components which causes regeneration of energy whereas deregulated autophagy exerts its implicated role in development and pathogenesis of auto-immune diseases such as rheumatoid arthritis. The immune, innate, and adaptive responses are regulated through the development, proliferation, and growth of lymphocytes. Such innate and adaptive responses can act as mediator of arthritis; along with this, stimulation of osteoclast-mediated bone resorption takes place via transferring citrullinated peptides towards MHC (major histocompatibility complex) compartments, thereby resulting in degradation of bone. Processes such as apoptosis resistance are also regulated through autophagy. In this review, the current knowledge based on role of autophagy in pathogenesis of rheumatoid arthritis is summarized along with proteins associated.

中文翻译：

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关注自噬在类风湿性关节炎中的多模式作用。

自噬在真核细胞中发挥其双重作用，并通过降解机制和调节分解代谢过程从而消除病原体来发挥其细胞保护作用。在合适的条件下，自噬与细胞质成分的再循环有关，导致能量再生，而失调的自噬在自身免疫性疾病（如类风湿性关节炎）的发展和发病机制中发挥相关作用。免疫、先天和适应性反应是通过淋巴细胞的发育、增殖和生长来调节的。这种先天的和适应性的反应可以作为关节炎的介质；与此同时，通过将瓜氨酸肽转移到 MHC（主要组织相容性复合体）区室来刺激破骨细胞介导的骨吸收，从而导致骨骼退化。细胞凋亡抗性等过程也通过自噬进行调节。在这篇综述中，基于自噬在类风湿性关节炎发病机制中的作用的当前知识与相关蛋白质一起进行了总结。