About this Research Topic
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 significant role. This is evident through the release of mitochondrial (mt) dsRNA and DNA, which have been found to trigger an interferon Type I response by interacting with their respective pattern recognition receptors (PPRs). Additionally, mt DNA can be released through vesicles containing mt DNA, which are directed to the lysosome. Therefore, disruptions in cell trafficking also have the potential to activate the Type I interferon pathway.
The presence of mitochondrial DNA in the cytosol and the subsequent activation of Type I interferon have been reported in diseases such as Huntington's disease, Parkinson's disease, ALS, and Friedreich Ataxia. However, the specific role and contribution of interferon-stimulated genes (ISGs) in these diseases remain largely unknown. Furthermore, it is not well understood whether this process can manifest in a chronic form. Activation of the Type I interferon response may sustain a state of chronic inflammation, potentially impacting the adaptive immune response and ultimately contributing to disease progression.
The aim of this research topic is to investigate the role of Type I interferon activation in the pathogenesis and progression of neurological diseases. We encourage original studies that contribute to our understanding in the following areas (but not limited to):
-Expanding our knowledge of diseases associated with Type I interferon response.
-Identifying the mechanisms behind the activation of the interferon pathway in specific diseases.
-Examining whether the Type I interferon response is tissue-, cell type-, or area-specific in particular diseases.
-Distinguishing how the activation of Type I interferon in a specific cell type may impact the microenvironment, neighboring cells, and the recruitment of other immune cells.
-Identifying potential points of pharmacological intervention to modulate the activation of this pathway.
This comprehensive exploration of Type I interferon activation and its implications in neurological diseases will contribute to advancing our understanding of disease mechanisms and potentially uncovering new therapeutic targets.
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 significant role. This is evident through the release of mitochondrial (mt) dsRNA and DNA, which have been found to trigger an interferon Type I response by interacting with their respective pattern recognition receptors (PPRs). Additionally, mt DNA can be released through vesicles containing mt DNA, which are directed to the lysosome. Therefore, disruptions in cell trafficking also have the potential to activate the Type I interferon pathway.
The presence of mitochondrial DNA in the cytosol and the subsequent activation of Type I interferon have been reported in diseases such as Huntington's disease, Parkinson's disease, ALS, and Friedreich Ataxia. However, the specific role and contribution of interferon-stimulated genes (ISGs) in these diseases remain largely unknown. Furthermore, it is not well understood whether this process can manifest in a chronic form. Activation of the Type I interferon response may sustain a state of chronic inflammation, potentially impacting the adaptive immune response and ultimately contributing to disease progression.
The aim of this research topic is to investigate the role of Type I interferon activation in the pathogenesis and progression of neurological diseases. We encourage original studies that contribute to our understanding in the following areas (but not limited to):
-Expanding our knowledge of diseases associated with Type I interferon response.
-Identifying the mechanisms behind the activation of the interferon pathway in specific diseases.
-Examining whether the Type I interferon response is tissue-, cell type-, or area-specific in particular diseases.
-Distinguishing how the activation of Type I interferon in a specific cell type may impact the microenvironment, neighboring cells, and the recruitment of other immune cells.
-Identifying potential points of pharmacological intervention to modulate the activation of this pathway.
This comprehensive exploration of Type I interferon activation and its implications in neurological diseases will contribute to advancing our understanding of disease mechanisms and potentially uncovering new therapeutic targets.
Keywords: Type I interferon, Innate immunity, Neurological Diseases, Interferon stimulated genes (ISG)
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
