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Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by coexisting processes of inflammation, demyelination, axonal neurodegeneration, and gliosis. It is the most common disabling neurological disease in young adulthood. Although autoimmune inflammation contributes to axonal pathology and demyelination, more recent evidence suggests that inflammation may also be beneficial. Protective autoimmunity is partly mediated via neurotrophic factors and neurotrophin regulation. Elevated neurotrophin levels have been observed during inflammatory processes, in MS lesions, whole peripheral blood mononuclear cells (PBMCs), serum, and cerebrospinal fluid (CSF). Furthermore, we recently demonstrated that T cells of MS patients produce neurotrophins (Soltys et al., 2014).

neural regeneration research/neural regeneration research

Interferon beta (IFN-β) treatment exerts potential neuroprotective effects through neurotrophic factors and novel neurotensin/neurotensin high affinity receptor 1 pathway