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An Important Role for Type III Interferon (IFN-λ/IL-28) in TLR-Induced Antiviral Activity1
TLDR
Type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs, and it is shown that TLR-activated antiviral defense requires expression of IL-28Rα only on nonhemopoietic cells. Expand
Proteasomal Degradation of Herpes Simplex Virus Capsids in Macrophages Releases DNA to the Cytosol for Recognition by DNA Sensors
TLDR
It is demonstrated that the HSV-1 capsid was ubiquitinated in the cytosol and degraded by the proteasome, hence releasing genomic DNA into the cytoplasm for detection by DNA sensors, which is important for induction of IFN-β in human macrophages postinfection with HSv-1 and CMV. Expand
TLR3 deficiency renders astrocytes permissive to herpes simplex virus infection and facilitates establishment of CNS infection in mice.
TLDR
It is shown that in mice TLR3 provides early control of HSV-2 infection immediately after entry into the CNS by mediating type I IFN responses in astrocytes, possibly preventing HSV from spreading beyond the neurons mediating entry intoThe CNS. Expand
Expression of Type III Interferon (IFN) in the Vaginal Mucosa Is Mediated Primarily by Dendritic Cells and Displays Stronger Dependence on NF-κB than Type I IFNs
TLDR
It is reported that different PAMPs induce type I and III IFN expression at different ratios after mucosal administration in the vaginas of mice and that Toll-like receptor 9 (TLR9) stimulation evokes a particularly strong IFN-λ response, which is essential for optimal antiviral protection. Expand
Mechanisms of type III interferon expression.
TLDR
It is proposed thatIFN-lambda expression is more flexible than IFN-alpha/beta expression, which could allow expression of type III IFNs in response to a wider range of stimuli compared with type I IFNs. Expand
SARS-CoV2-mediated suppression of NRF2-signaling reveals potent antiviral and anti-inflammatory activity of 4-octyl-itaconate and dimethyl fumarate
TLDR
NRF2 agonists 4-OI and DMF induce a distinct IFN-independent antiviral program that is broadly effective in limiting virus replication and in suppressing the pro-inflammatory responses of human pathogenic viruses, including SARS-CoV2. Expand
An innate antiviral pathway acting before interferons at epithelial surfaces
TLDR
An innate antiviral pathway is identified that works at epithelial surfaces before the classical IFN response is operative, activated independently of known innate sensors of viral infections through a mechanism dependent on viral O-linked glycans. Expand
Nrf2 negatively regulates STING indicating a link between antiviral sensing and metabolic reprogramming
TLDR
Nrf2 activation decreases STING expression and responsiveness to STING agonists while increasing susceptibility to infection with DNA viruses, and a link between metabolic reprogramming and antiviral cytosolic DNA sensing in human cells is suggested. Expand
Extracellular superoxide dismutase is present in secretory vesicles of human neutrophils and released upon stimulation.
TLDR
The data signifies that EC-SOD released from activated neutrophils affects the redox conditions of the extracellular space and may offer protection against highly reactive oxygen species such as hydroxyl radicals otherwise generated as a result of respiratory burst activity of activated Neutrophils. Expand
Nitro-fatty acids are formed in response to virus infection and are potent inhibitors of STING palmitoylation and signaling
TLDR
It is reported that endogenously formed nitro-fatty acids can covalently modify STING by Nitro-alkylation, and proposed that these lipids could have pharmaceutical potential for treatment of STING-dependent inflammatory diseases. Expand
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