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Status |
Public on Oct 14, 2020 |
Title |
A critical role for STING signaling in limiting pathogenesis of Chikungunya virus |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
The stimulator-of-interferon-gene (STING) pathway controls both DNA and RNA virus infection. STING is essential for induction of innate immune responses during DNA virus infection, while its mechanism against RNA virus remains largely elusive. We show that STING signaling is crucial for restricting Chikungunya virus infection and arthritis pathogenesis. Sting-deficient mice (Stinggt/gt) had elevated viremia throughout the viremic stage and viral burden in the feet transiently, along with a normal type I IFN response. Stinggt/gt mice presented much greater foot swelling, joint damage and immune cell infiltration than WT mice. Intriguingly, expression of interferon gamma and its induced Cxcl10 was continuously upregulated by ~7-10-fold, and further elevated in Stinggt/gt mice synchronously with arthritis progression. However, expression of chemoattractants for and activators of neutrophils, Cxcl5, Cxcl7 and Cxcr2 was suppressed in Stinggt/gt joints. These results demonstrate that STING deficiency leads to an aberrant chemokine response that promotes pathogenesis of CHIKV arthritis.
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Overall design |
Bone-marrow-derived macrophages from three individual WT/Sting gt/gt mice were infected by CHIKV at a multiplicity of infection of 5 for 12 hrs or not infected (mock). The whole genome transcriptome was analyzed by RNAseq.
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Contributor(s) |
Geng T, Wang P |
Citation missing |
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Submission date |
Oct 13, 2020 |
Last update date |
Oct 20, 2020 |
Contact name |
Tingting Geng |
E-mail(s) |
geng@uchc.com
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Organization name |
Uconn Health
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Department |
Department of Immunology
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Lab |
Penghua Wang
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Street address |
263 Farmington Avenue
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City |
Farmington |
State/province |
CT |
ZIP/Postal code |
06030 |
Country |
USA |
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Platforms (1) |
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Samples (12)
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Relations |
BioProject |
PRJNA668984 |
SRA |
SRP287249 |