Type I Interferon Activation in Neurological Diseases
Innate immunity, serving as the initial defense mechanism in an organism following a bacterial or viral infection, involves multiple pattern recognition receptors (PRRs) present in the plasma membranes, endosomes, and cytosol. These PRRs are responsible for recognizing the presence of foreign nucleic acids. The activation of the single-stranded RNA cytosolic sensor (Retinoic acid-inducible-I-like receptors or RIG-I) or the double-stranded RNA cytosolic sensor (MDA5) and the DNA cytosolic sensors (cGAS) leads to the transcription of Type I interferon and subsequently, the Interferon-stimulated genes (ISGs). These events play a crucial role in combating pathogen replication, contributing to local inflammation, and facilitating the recruitment of other cells from the adaptive immune system. Recent discoveries have shed light on the involvement of cell-intrinsic events in the upregulation of Type I interferon. Among the various mechanisms identified, mitochondrial dysfunction plays a signi