Author Correction: STEEP mediates STING ER exit and activation of signaling.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

STEEP mediates STING ER exit and activation of signaling.

STING is essential for control of infections and for tumor immunosurveillance, but it can also drive pathological inflammation. STING resides on the endoplasmic reticulum (ER) and traffics following stimulation to the ERGIC/Golgi, where signaling occurs. Although STING ER exit is the rate-limiting step in STING signaling, the mechanism that drives this process is not understood.

inveSTING in a latent future.

is an obligate protozoan parasite that naturally infects all mammals, where it alters the host environment to establish chronic infection. Wang and colleagues uncover a new role for the protein GRA15 in inducing an anti-parasite response via the interferon stimulator STING. This parasite-driven host defense limits replication while maintaining host survival, creating an ideal niche for the establishment of latency.

Intercellular communication in the innate immune system through the cGAS-STING pathway.

Type I interferons (IFNα/β) are pivotal to anti-viral defense. Although an absolute requirement for viral clearance, the presence of IFN in high doses sustained over time has been implicated to be the underlying cause of clinical outcomes such as interferonopathies. Therefore, tight regulation of cellular communication processes is required for tissue homeostasis.

Sensing of HSV-1 by the cGAS-STING pathway in microglia orchestrates antiviral defence in the CNS.

Herpes simplex encephalitis (HSE) is the most common form of acute viral encephalitis in industrialized countries. Type I interferon (IFN) is important for control of herpes simplex virus (HSV-1) in the central nervous system (CNS). Here we show that microglia are the main source of HSV-induced type I IFN expression in CNS cells and these cytokines are induced in a cGAS-STING-dependent manner.

Lack of immunological DNA sensing in hepatocytes facilitates hepatitis B virus infection.

Unlabelled: Hepatitis B virus (HBV) is a major human pathogen, and about one third of the global population will be exposed to the virus in their lifetime. HBV infects hepatocytes, where it replicates its DNA and infection can lead to acute and chronic hepatitis with a high risk of liver cirrhosis and hepatocellular carcinoma. Despite this, there is limited understanding of how HBV establishes chronic infections.

Catching the adaptor-WDFY1, a new player in the TLR-TRIF pathway.

The innate immune system detects microbes and abnormal self through pattern recognition receptors (PRRs), which detect molecules that are either specific for microbes (such as lipopolysaccharide), present in much higher concentrations during infection (such as double-stranded RNA), or present in aberrant locations (such as cytosolic DNA) [1]. The Toll-like receptors (TLRs) are the best-described set of PRRs. TLRs are membrane-bound receptors localized on the plasma membrane and in endosomes, the ligand-binding regions of which face the extracellular environment and the endosomal lumen, respectively [1].

Hepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms.

Background & Aims: Current treatment strategies for hepatitis C virus (HCV) infection include pegylated interferon (IFN)-alfa and ribavirin. Approximately 50% of patients control HCV infection after treatment, but the broad range of patients' outcomes and responses to treatment, among all genotypes, indicates a role for host factors. Although the IFN system is important in limiting HCV replication, the virus has evolved mechanisms to circumvent the IFN response.

Utility of saliva and hair follicles in donor selection for hematopoietic stem cell transplantation and chimerism monitoring.

Selection of an HLA identical donor is a critical pre-requisite for successful hematopoietic stem cell transplantation (HSCT). Most transplant centers utilize blood as the most common source of DNA for HLA testing. However, obtaining blood through phlebotomy is often challenging in patients with conditions like severe leucopenia or hemophilia, pediatric and elderly patients.

IRF-1 expression is essential for natural killer cells to suppress metastasis.

IFN-γ promotes tumoral immune surveillance, but its involvement in controlling metastases is less clear. Using a mouse model of pulmonary metastases, we show that local IFN-γ treatment inhibits formation of metastases through its regulation of IRF-1 in tumor cells. IRF-1 is an IFN-γ-induced transcription factor pivotal in the regulation of infection and inflammation.