Ganciclovir attenuates the onset and progression of experimental autoimmune uveitis by inhibiting infiltration of Th17 and inflammatory cells into the retina

Lin, Xiangxiang; Shang, Huiping; Zhu, Yutuo; Chen, Jinrun; Deng, Mengyun; Lin, Dan; Vakal, Serhii; Li, Xingyi

doi:10.1016/j.bcp.2022.114917

Cited by 6 publications

(1 citation statement)

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“…Indeed, several lines of evidence have suggested the involvement of cGAS-STING signaling in the pathogenesis of autoimmune uveitis. For example, STING protein was recently found upregulated in infiltrating T cells and inflammatory cells as well as retinal glial cells in the EAU model [ 85 ], suggesting cGAS-STING signaling may be upregulated to mediate priming and infiltration of immune cells into the retina to contribute to the pathogenesis of autoimmune uveitis. In contrast, type I IFN (IFN-α/β) from STING signaling was documented to unexpectedly alleviate autoimmune uveitis in the EAU model via hindering IFN-γ-producing pathogenic CD4 + effector T cells in the spleen from migrating into the effector sites in the eyes in a manner dependent on the downregulation of CXCR3 expression, which resulted from type I IFN-stimulated overproduction of CXCR3 cognate ligands (CXCL9, CXCL10, and CXCL11) [ 24 ].…”

Section: Cgas-sting Signaling In Uveitismentioning

confidence: 99%

Emerging Roles of cGAS-STING Signaling in Mediating Ocular Inflammation

Zhou,

Ho,

Chan

et al. 2023

J Innate Immun

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Cyclic GMP-AMP (cGAMP) synthase (cGAS), a sensor of cytosolic DNA, recognizes cytoplasmic nucleic acids to activate the innate immune responses via generation of the second messenger cGAMP and subsequent activation of the stimulator of interferon genes (STING). The cGAS–STING signaling has multiple immunologic and physiological functions in all human vital organs. It mediates protective innate immune defense against DNA-containing pathogen infection, confers intrinsic antitumor immunity via detecting tumor-derived DNA, and gives rise to autoimmune and inflammatory diseases upon aberrant activation by cytosolic leakage of self-genomic and mitochondrial DNA. Disruptions in these functions are associated with the pathophysiology of various immunologic and neurodegenerative diseases. Recent evidence indicates important roles of the cGAS-STING signaling in mediating inflammatory responses in ocular inflammatory and inflammation-associated diseases, such as keratitis, diabetic retinopathy, age-related macular degeneration, and uveitis. In this review, we summarize the recently emerging evidence of cGAS-STING signaling in mediating ocular inflammatory responses and affecting pathogenesis of these complex eye diseases. We attempt to provide insightful perspectives on future directions of investigating cGAS-STING signaling in ocular inflammation. Understanding of how cGAS-STING signaling is modulated to mediate ocular inflammatory responses would allow future development of novel therapeutic strategies to treat ocular inflammation and autoimmunity.

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Section: Cgas-sting Signaling In Uveitismentioning

confidence: 99%