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

ABSTRACT:

Objective

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.

Methods

Bone parameters were evaluated by micro-computed tomography and histomorphometry in DKO mice in comparison with mice triple deficient in STING, DNase II, and IFNAR and co

SUBMITTER: Baum R 

PROVIDER: S-EPMC5274601 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature