Targeting the NLRP3 inflammasome and associated cytokines in scleroderma associated interstitial lung disease

Frontiers in Cell and Developmental Biology

Cell and Developmental Biology

Alexander Ghincea¹  Shifa Gandhi¹  Samuel Woo¹  Tina Saber¹  Chris J. Lee¹  Changwan Ryu² 

[1] Department of Internal Medicine, Yale School of Medicine, Section of Pulmonary, Critical Care and Sleep Medicine, New Haven, CT, United States;null;

关键词: scleroderma associated interstitial lung disease;    NLRP3;    tumor necrosis factor;    alpha;    IL-1 beta;    IL-18;   

DOI  :  10.3389/fcell.2023.1254904

 received in 2023-07-07, accepted in 2023-09-19,  发布年份 2023

来源: Frontiers

【 摘 要 】

SSc-ILD (scleroderma associated interstitial lung disease) is a complex rheumatic disease characterized in part by immune dysregulation leading to the progressive fibrotic replacement of normal lung architecture. Because improved treatment options are sorely needed, additional study of the fibroproliferative mechanisms mediating this disease has the potential to accelerate development of novel therapies. The contribution of innate immunity is an emerging area of investigation in SSc-ILD as recent work has demonstrated the mechanistic and clinical significance of the NLRP3 inflammasome and its associated cytokines of TNFα (tumor necrosis factor alpha), IL-1β (interleukin-1 beta), and IL-18 in this disease. In this review, we will highlight novel pathophysiologic insights afforded by these studies and the potential of leveraging this complex biology for clinical benefit.

【 授权许可】

Unknown   
Copyright © 2023 Woo, Gandhi, Ghincea, Saber, Lee and Ryu.