Sarcoidosis is an enigmatic multisystem disease characterized by the development and accumulation of granulomas: a compact collection of macrophages that have differentiated into epithelioid cells and which are associated with T helper (Th)1 and Th17 cells. Although no single causative factor has been shown to underlie sarcoidosis in humans, its etiology has been related to microbial, environmental, and genetic factors. We examine how these factors play a role in sarcoidosis pathogenesis. Specifically, we propose that dysfunction of mTOR, Rac1, and autophagy-related pathways not only hampers pathogen or nonorganic particle clearance but also participates in T cell and macrophage dysfunction, driving granuloma formation. This concept opens new avenues for potentially treating sarcoidosis and may serve as a blueprint for other granulomatous disorders.

中文翻译：

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结节病和 mTOR、Rac1 和自噬三联征。

肉瘤病是一种神秘的多系统疾病，其特征是肉芽肿的发生和积累：已分化为上皮样细胞并与 T 辅助 (Th)1 和 Th17 细胞相关的巨噬细胞的紧凑集合。虽然没有单一的致病因素被证明是人类结节病的基础，但其病因与微生物、环境和遗传因素有关。我们研究了这些因素如何在结节病的发病机制中发挥作用。具体来说，我们提出 mTOR、Rac1 和自噬相关通路的功能障碍不仅会阻碍病原体或非有机颗粒清除，还会参与 T 细胞和巨噬细胞功能障碍，从而导致肉芽肿形成。