Peripheral neuropathy refers to an array of neurodegenerative diseases in the peripheral nervous system (PNS), involving damage or loss of axonal structures. It strikes millions of patients worldwide, who would suffer debilitating deficits such as chronic pain, numbness, weakness, paralysis, or even death. Commonly occurring neurological conditions, e.g., traumatic nerve injuries, chemotherapy-induced peripheral neuropathy, diabetic peripheral neuropathy, and Guillain-Barre syndrome, have been extensively investigated for their pathological mechanisms. In the past decade, we have witnessed exciting discoveries that begin to elucidate specific signaling molecules designated for axonal destruction or repair in the PNS, offering hopes of preventing and eventually curing these dreadful diseases.
As one of the frontiers of ongoing research in the field, it has become increasingly evident that reciprocal interactions between the PNS and the immune system determine the outcomes of peripheral neuropathy. For instance, it has been well recognized that axonal degeneration in traumatically-injured nerves triggers the recruitment of monocytes and macrophages, which in turn would clear tissue debris and facilitate the later process of axonal regeneration. Similarly, self-antigens released from damaged nerves may augment the adaptive immunity that produces auto-reactive antibodies, further destructing myelin sheath in Guillain-Barre syndrome. Also, studies have documented a collection of immune cytokines or chemokines that critically contribute to the onset and persistence of chronic pain under a variety of neuropathic conditions.
Given the complexity of peripheral neuropathy, significant gaps in the current knowledge remain and call for research efforts. This Research Topic is designated to welcome both Reviews and Original Research Articles that focus on the basic cellular and molecular mechanisms underlying neuroimmune interactions in peripheral neuropathy. We believe that this collection of publications would help promote our better understanding of peripheral neuropathy, and at the same time, highlight a path for future interdisciplinary research.
Several important aspects deserve our focused attention, including but not limited to:
- Investigating molecular pathways underlying the communication between the PNS and the immune system;
- Exploring molecular and cellular mechanisms involving the interactions between peripheral non-neuronal cells (e.g., glia, fibroblasts, and endothelial cells) and immune system;
- Unrecognized types of peripheral neuropathy, beyond aforementioned and commonly-studied scenarios, and its potential relation to the broadly-defined neuroimmune interplay in diseases.
Peripheral neuropathy refers to an array of neurodegenerative diseases in the peripheral nervous system (PNS), involving damage or loss of axonal structures. It strikes millions of patients worldwide, who would suffer debilitating deficits such as chronic pain, numbness, weakness, paralysis, or even death. Commonly occurring neurological conditions, e.g., traumatic nerve injuries, chemotherapy-induced peripheral neuropathy, diabetic peripheral neuropathy, and Guillain-Barre syndrome, have been extensively investigated for their pathological mechanisms. In the past decade, we have witnessed exciting discoveries that begin to elucidate specific signaling molecules designated for axonal destruction or repair in the PNS, offering hopes of preventing and eventually curing these dreadful diseases.
As one of the frontiers of ongoing research in the field, it has become increasingly evident that reciprocal interactions between the PNS and the immune system determine the outcomes of peripheral neuropathy. For instance, it has been well recognized that axonal degeneration in traumatically-injured nerves triggers the recruitment of monocytes and macrophages, which in turn would clear tissue debris and facilitate the later process of axonal regeneration. Similarly, self-antigens released from damaged nerves may augment the adaptive immunity that produces auto-reactive antibodies, further destructing myelin sheath in Guillain-Barre syndrome. Also, studies have documented a collection of immune cytokines or chemokines that critically contribute to the onset and persistence of chronic pain under a variety of neuropathic conditions.
Given the complexity of peripheral neuropathy, significant gaps in the current knowledge remain and call for research efforts. This Research Topic is designated to welcome both Reviews and Original Research Articles that focus on the basic cellular and molecular mechanisms underlying neuroimmune interactions in peripheral neuropathy. We believe that this collection of publications would help promote our better understanding of peripheral neuropathy, and at the same time, highlight a path for future interdisciplinary research.
Several important aspects deserve our focused attention, including but not limited to:
- Investigating molecular pathways underlying the communication between the PNS and the immune system;
- Exploring molecular and cellular mechanisms involving the interactions between peripheral non-neuronal cells (e.g., glia, fibroblasts, and endothelial cells) and immune system;
- Unrecognized types of peripheral neuropathy, beyond aforementioned and commonly-studied scenarios, and its potential relation to the broadly-defined neuroimmune interplay in diseases.