In addition to mTOR and JAK/STAT, NLRP3 inflammasome is another key pathway activated in sarcoidosis

[摘要] Sarcoidosis is a rare “old disease” first described over a century ago, known as a multifaceted systemic multiorgan inflammatory granulomatosis characterised by the presence of non-necrotising epithelioid granulomas [1, 2]. In many ways sarcoidosis remains a mysterious disease with numerous unsolved knowledge gaps. The still unknown aetiology/aetiologies of sarcoidosis is one of these gaps, i.e. the disease develops in genetically predisposed individuals following as-yet-unknown antigen exposure. Various triggers or causes have been suspected, including bacterial agents (such as Propionibacterium acnes or mycobacterial antigens) or environmental particulates (such as crystalline silica), but their true identity and mechanisms of action are still not elucidated [1–3]. The second main gap regards the nature of the granuloma foundation, the hallmark of the disease, as its mechanisms related to complex immunopathogenesis are only partially understood [1–3]. Furthermore, even though the highly variable course of the disease is well documented, disease evolution is still quite unpredictable for a given patient. In many cases, tissue granulomas resolve spontaneously, while in others they persist or reoccur and require treatment; usually prednisone alone, or other drugs such as immunosuppressants [1, 2, 4]. The current therapeutic monitoring is hence mainly based on empirical knowledge and not on well-identified pathogenesis mechanisms. Therefore, a better knowledge of the intracellular pathways potentially activated is needed.

[学科分类] 呼吸医学