STING Contributes to Abnormal Bone Formation Induced by Deficiency of DNase II in Mice

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• 作者：Rebecca Baum ; Shruti Sharma ; Jason M. Organ ; Christopher Jakobs ; Veit Hornung ; David B. Burr ; Ann Marshak-Rothstein ; Katherine A. Fitzgerald and Ellen M. Gravallese
• 刊名：Arthritis & Rheumatism
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：69
• 期：2
• 页码：460-471
• 全文大小：919K
• ISSN：1529-0131

文摘

Cytosolic DNA sensors detect microbial DNA and promote type I interferon (IFN) and proinflammatory cytokine production through the adaptor stimulator of IFN genes (STING) to resolve infection. Endogenous DNA also engages the STING pathway, contributing to autoimmune disease. This study sought to identify the role of STING in regulating bone formation and to define the bone phenotype and its pathophysiologic mechanisms in arthritic mice double deficient in DNase II and IFN-α/β/ω receptor (IFNAR) (DNase II^−/−/IFNAR^−/− double-knockout [DKO] mice) compared with controls.