Multiple sclerosis (MS) and traumatic axonal injuries both involve the central nervous system (CNS) being compromised by immune system attacks, leading to inflammation, demyelination, and neurological dysfunction. Understanding the immunopathogenesis of these conditions is crucial for developing effective treatments.
In MS, an autoimmune disorder, the immune system mistakenly targets myelin, the protective layer around nerve fibers in the CNS. Both adaptive and innate immunity play roles in its 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.
Deepening our understanding of MS and axonal injury immunopathogenesis offers potential for identifying novel therapeutic targets and creating personalized treatments. Current research explores immune cell subsets, neuroprotective strategies, and innovative therapies like antigen-specific tolerance 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 and Review articles are welcome.
Keywords: Immunopathogenesis, Multiple Sclerosis, Innovative Treatments
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.
