Stimulator of interferon genes (STING), also known as TMEM173, promotes the production of the interferon’s IFN-alpha and IFN-beta. STING possesses three functional domains: a cytoplasmic C-terminal tail, a central globular domain, and four N-terminal transmembrane motifs that attach it to the ER. The role of STING in the immune response is specific to its ability to sense nucleic acids, particularly dsDNA. When STING is over induced, the protein IRF3 undergoes a nuclear translocation resulting in IFN induction, which in turn activates the innate immune response. The herpes virus is a DNA based virus targeted to DNA-sensing pathways that has the capacity to elicit latent recurrent infections on a host. Because of the overlap between the herpes virus affecting DNA-sensing and the ability of STING to sense nucleic acids, using STING antibodies in herpes simplex virus research is an effective way to further elucidate its role.
STING/TMEM173 Antibody [NBP2-24683] - IHC analysis of STING in formalin-fixed paraffin-embedded human colon cancer tissue section using STING antibody at 1:100 dilution with detection employing HRP-conjugated secondary antibody. The signal was developed using DAB reagent and the nuclei were counterstained with hematoxylin. The antibody generated very weak cytoplasmic staining in columner epithelial cells with a very strong signal in the secretory/goblet cells.
First, Sun C et al used a STING antibody in their research to investigate how the evasion of innate cytosolic DNA sensing by the gamma herpes virus may be responsible for latent infection. To begin, Sun C et al wanted to establish that herpes viruses did in fact induce the innate immune response, so they tested the effects that a lack of STING had on infection by MHV68. Next, the STING antibody was used on HSV infected THP1-cells in fluorescent immunohistochemistry and subsequently analyzed by confocal microscopy to show that KSHV induces the expression of IFB-beta independent of STING. To confirm this, neither STING nor IFI16 translocated after infection with HCMV. Overall, the ability for a host to control infection of the HSV after induction is very necessary for the prevention of the disease. With this research, it is clear that both the innate and adaptive immune response work to manage the HSV.
Next, Reinert et al used a STING antibody to better understand how sensing of HSV-1 by the cGAS-STING pathway in microglia may orchestrate antiviral defenses in the central nervous system. While Sun C et al used a STING antibody to examine gamma herpes virus, this group is specifically studying herpes simplex encephalitis (HSE), which also relies on interferons for its control. For starters, they established that mice lacking the STING protein are more susceptible to HSE, even showing a higher viral load of HSV-1 replication in STING 1 deficient microglia. To further elucidate the role of STING 1 in the CNS pathway in regards to HSV-1 infection, a STING1 antibody was used in immunofluorescence on astrocytes and microglia infected with HSV-1. These results confirmed that interferon production happened in a STING dependent manner.
