About this Research Topic
Multiple sclerosis (MS), a chronic autoimmune disease, and traumatic axonal injuries are both characterized by the immune system attacking the central nervous system (CNS), leading to inflammation, demyelination, and ultimately neurological dysfunction. Understanding the immunopathogenesis of MS and axonal injuries is crucial for developing effective treatments. MS is considered an autoimmune disorder where the immune system mistakenly attacks myelin, the protective sheath surrounding nerve fibers in the CNS. Both the adaptive and innate immune systems play roles in MS pathogenesis. Activated T cells, particularly CD4+ T cells, migrate into the CNS and initiate an inflammatory cascade, recruiting other immune cells and causing damage to myelin.
On the other hand, axonal injuries are characterized by an unresolved inflammatory phase that often leads to secondary damage and hinders axonal regeneration and functional recovery. Various pro-inflammatory cytokines and chemokines, such as interferon-gamma (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α), contribute to the inflammatory process in MS. These molecules promote immune cell activation, migration across the blood-brain barrier, and tissue damage within the CNS.
In the case of axonal injuries, normal wound healing is tightly orchestrated through sequential activation of distinct cytokines, however, after axonal injury, phase I proinflammatory cytokines (IL-1β, TNFα) persist over time, leading to inefficient phase transitions, phenotype shifts thereby hindering proper regeneration and healing. Demyelination, the loss of myelin sheath, is a hallmark feature of MS lesions.
Additionally, both after traumatic and autoimmune demyelinating injuries, neurons undergo axonal damage and neurodegeneration, contributing to the lack of functional recovery after traumatic axonal injuries and progressive disability observed in many MS patients. While inflammation initially drives secondary damage and demyelination, chronic neuroinflammation and neurodegeneration may persist even in the absence of overt immune activity.
Advancing our understanding of MS immunopathogenesis and axonal injuries holds promise for identifying novel therapeutic targets and developing more personalized treatment approaches. Research efforts focus on elucidating the role of specific immune cell subsets, investigating neuroprotective and neurodegenerative strategies, as well as exploring innovative therapies such as antigen-specific tolerance induction and stem cell transplantation.
In this research topic, we aim to comprehensively cover all relevant information about the recent advancement in immunopathogenesis in MS and traumatic axonal injuries.
Furthermore, we will explore how targeting a specific immune subset may have a potential implication in neuroprotective effects, which could serve as a key strategy for developing potential therapeutic interventions.
Original research articles and reviews are welcome.
On the other hand, axonal injuries are characterized by an unresolved inflammatory phase that often leads to secondary damage and hinders axonal regeneration and functional recovery. Various pro-inflammatory cytokines and chemokines, such as interferon-gamma (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α), contribute to the inflammatory process in MS. These molecules promote immune cell activation, migration across the blood-brain barrier, and tissue damage within the CNS.
In the case of axonal injuries, normal wound healing is tightly orchestrated through sequential activation of distinct cytokines, however, after axonal injury, phase I proinflammatory cytokines (IL-1β, TNFα) persist over time, leading to inefficient phase transitions, phenotype shifts thereby hindering proper regeneration and healing. Demyelination, the loss of myelin sheath, is a hallmark feature of MS lesions.
Additionally, both after traumatic and autoimmune demyelinating injuries, neurons undergo axonal damage and neurodegeneration, contributing to the lack of functional recovery after traumatic axonal injuries and progressive disability observed in many MS patients. While inflammation initially drives secondary damage and demyelination, chronic neuroinflammation and neurodegeneration may persist even in the absence of overt immune activity.
Advancing our understanding of MS immunopathogenesis and axonal injuries holds promise for identifying novel therapeutic targets and developing more personalized treatment approaches. Research efforts focus on elucidating the role of specific immune cell subsets, investigating neuroprotective and neurodegenerative strategies, as well as exploring innovative therapies such as antigen-specific tolerance induction and stem cell transplantation.
In this research topic, we aim to comprehensively cover all relevant information about the recent advancement in immunopathogenesis in MS and traumatic axonal injuries.
Furthermore, we will explore how targeting a specific immune subset may have a potential implication in neuroprotective effects, which could serve as a key strategy for developing potential therapeutic interventions.
Original research articles and reviews are welcome.
Keywords: Immunopathogenesis, Multiple Sclerosis, Innovative Treatments
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