RNA sensing via the RIG-I-like receptor LGP2 is essential for the induction of a type I IFN response in ADAR1 deficiency.

RNA editing by the adenosine deaminase ADAR1 prevents innate immune responses to endogenous RNAs. In ADAR1-deficient cells, unedited self RNAs form base-paired structures that resemble viral RNAs and inadvertently activate the cytosolic RIG-I-like receptor (RLR) MDA5, leading to an antiviral type I interferon (IFN) response. Mutations in ADAR1 cause Aicardi-Goutières Syndrome (AGS), an autoinflammatory syndrome characterized by chronic type I IFN production.

CD200R1L is a functional evolutionary conserved activating receptor in human neutrophils.

Inhibitory and activating immune receptors play a key role in modulating the amplitude and duration of immune responses during infection and in maintaining immune balance in homeostatic conditions. The CD200 Receptor (CD200R) gene family in humans encodes one inhibitory receptor, CD200R1, and one putative activating member, CD200R1 Like (CD200R1L). It is demonstrated that CD200R1L is endogenously expressed by human neutrophils and activates cellular functions such as reactive oxygen species (ROS) production via Syk, PI3Kβ, PI3Kδ, and Rac GTPase signaling.

Self RNA Sensing by RIG-I-like Receptors in Viral Infection and Sterile Inflammation.

The innate immune system uses pattern recognition receptors to survey the intracellular and extracellular environment for signs of infection. Viral infection is detected through the presence of viral nucleic acids in infected cells. Pattern recognition receptor activation by viral nucleic acids induces the expression and secretion of type I IFNs (IFN-Is), important mediators of antiviral immunity.

Can Patrolling Liver-Resident T Cells Control Human Malaria Parasite Development?

Recently, a population of non-recirculating, tissue-resident memory CD8 T cells has been identified; cells that seems to act as key sentinels for invading microorganisms with enhanced effector functions. In malaria, the liver represents the first site for parasite development before a definite infection is established in circulating red blood cells. Here, we discuss the evidence obtained from animal models on several diseases and hypothesize that liver-resident memory CD8 T cells (hepatic T) play a critical role in providing protective liver-stage immunity against Plasmodium malaria parasites.