Oliviero Francesca, Bindoli Sara, Scanu Anna, Feist Eugen, Doria Andrea, Galozzi Paola, Sfriso Paolo
Rheumatology Unit, Department of Medicine-DIMED, University of Padova, Padova, Italy.
Department of Rheumatology, Cooperation Partner of the Otto-von-Guericke, University Magdeburg, Helios Clinic, Vogelsang-Gommern, Germany.
Front Med (Lausanne). 2020 Apr 30;7:166. doi: 10.3389/fmed.2020.00166. eCollection 2020.
Crystal-induced arthritides have been classified as "type-1 autoinflammatory diseases" for their main features which resemble those of the monogenic autoinflammatory syndromes. They are in fact characterized by spontaneous onset, recurrence of the episodes, self-limitation and resolution, inflammasome activation with huge production of IL-1β and a prevalent involvement of the innate immune system. The term "auto" refers also to the induction of IL-1β gene expression, processing and secretion by IL-1β itself. The concept of autoinflammation in crystal-induced arthritis has been finally reinforced by the efficacy of IL-1 blockade in treating acute and chronic state of this disease. The aim of this article is to review the autoinflammatory mechanisms in crystal-induced arthritis, considering both clinical and molecular aspects.
晶体诱导的关节炎因其主要特征与单基因自身炎症综合征相似,已被归类为“1型自身炎症性疾病”。事实上,它们的特点是起病自发、发作反复、自限性及缓解、炎性小体激活并大量产生白细胞介素-1β(IL-1β),且固有免疫系统受累为主。“自身”一词也指IL-1β自身对IL-1β基因表达、加工及分泌的诱导。IL-1阻断剂治疗该疾病急慢性状态的疗效最终强化了晶体诱导性关节炎中自身炎症的概念。本文旨在从临床和分子方面综述晶体诱导性关节炎中的自身炎症机制。