Biotech Values

[genisi]

On Multiple Sclerosis

The classical concept that MS is a TH1 (T helper1) cell-mediated autoimmune disease is being challenged by evidence that other adaptive immune cells (such as TH17 cells and peripheral b lymphocytes), as well as key innate immune cells (dendritic cells, natural killer T cells and resident microglia), also play a significant role in MS pathogenesis. A new notion that adaptive immunity may be involved in RRMS, while specific innate immunity dysfunction may relate to disease progression, is arising. Under this view, disease progression may relate to an immune balance shift that is characterized by abnormal activation of innate immune effectors: active inflammation may determine the initial disease course, but disease progression takes place independently of acute inflammation but dysregulation of the innate immune system is a key factor involved in the shift towards irreversible neurodegeneration and MS progression. CNS inflammation is independent from axonal loss and neurodegeneration, with the latter being crucial factors implicated in disease progression and disability.
This hypothesis may in part explain why currently approved MS therapies with anti-inflammatory mechanisms that target the adaptive immune system show little effect in progressive stages.