The Agreement between Radiography and Fluoroscopy as Diagnostic Tools for Tracheal Collapse in Dogs.

Tracheal collapse is a common disease in small, middle-aged dogs, and imaging tools are essential for its diagnosis. Radiography and fluoroscopy are the main diagnostic modalities used, but their agreement in different regions is not well documented. In this study, the agreement between thoracic radiography and fluoroscopy in tracheal collapse was investigated in 29 dogs. The results showed that radiography detected a lower degree of collapsing trachea compared to fluoroscopy at the carina region (p < 0.001). However, there was no significant difference observed between the degree of collapsing trachea detected by radiography and fluoroscopy at the cervical, thoracic inlet, and intra-thoracic regions (p = 0.780, 0.537, and 0.213, respectively). The kappa statistic indicated a slight agreement at the cervical region at a 16.4% cut-off (κ = 0.20), while the other regions showed a non-agreement. In conclusion, although radiography is useful for screening, fluoroscopy was able to detect the degree of the collapsing trachea greater than radiography in the carina region. Additionally, if a collapse in the cervical region is detected by radiography, it is prone to have a positive relationship with fluoroscopy as well.

Erratum: STING Mediates Lupus via the Activation of Conventional Dendritic Cell Maturation and Plasmacytoid Dendritic Cell Differentiation.

[This corrects the article DOI: 10.1016/j.isci.2020.101530.].

STING Mediates Lupus via the Activation of Conventional Dendritic Cell Maturation and Plasmacytoid Dendritic Cell Differentiation.

Signaling through stimulator of interferon genes (STING) leads to the production of type I interferons (IFN-Is) and inflammatory cytokines. A gain-of-function mutation in STING was identified in an autoinflammatory disease (STING-associated vasculopathy with onset in infancy; SAVI). The expression of cyclic GMP-AMP, DNA-activated cGAS-STING pathway, increased in a proportion of patients with SLE. The STING signaling pathway may be a candidate for targeted therapy in SLE. Here, we demonstrated that disruption of STING signaling ameliorated lupus development in Fcgr2b-deficient mice. Activation of STING promoted maturation of conventional dendritic cells and differentiation of plasmacytoid dendritic cells via LYN interaction and phosphorylation. The inhibition of LYN decreased the differentiation of STING-activated dendritic cells. Adoptive transfer of STING-activated bone marrow-derived dendritic cells into the FCGR2B and STING double-deficiency mice restored lupus phenotypes. These findings provide evidence that the inhibition of STING signaling may be a candidate targeted treatment for a subset of patients with SLE.

Deficiency of STING Promotes Collagen-Specific Antibody Production and B Cell Survival in Collagen-Induced Arthritis.

The levels of interferon-alpha are high in the serum and synovial fluid of rheumatoid arthritis (RA) patients. Activation of the stimulator of type I interferon genes (STING) mediates the productions of type I interferon and promotes chronic inflammation. STING plays a significant role in autoimmune lupus mice. However, the function of STING in collagen-induced arthritis (CIA) model has never been described. This study aimed to test the function of STING in CIA. The Sting-deficient mice developed arthritis comparable to WT mice. The levels of anti-collagen antibody from Sting-deficient mice were significantly higher than the WT mice. The B cells derived from Sting-deficient mice showed better survival than WT mice in response to the B cell receptor (BCR) stimulation. Activation of STING also induced B cell death, especially in activated B cells. This study demonstrated that the inhibition of STING promotes anti-collagen antibodies and B cell survival, which suggested that STING acts as a negative regulator of B cell function in the CIA model.