FIGURE 2 | Multiple sclerosis immunopathogenesis and therapeutic targets.

Immature dendritic cells are central players in innate immune responses and are involved in the maintenance of peripheral tolerance by means of promotion of suppressor regulatory T cell and anti-inflammatory T helper 2 (T_H2) cell responses. Abnormally activated (mature) antigen-presenting dendritic cells can be found in patients with multiple sclerosis (MS). This activation results in increased production of pro-inflammatory cytokines that lead to aberrant activation of T_H1 and T_H17 pro-inflammatory responses. Activated encephalitogenic adaptive immune effectors (such as T_H1 cells, T_H17 cells, CD8⁺ cells and B cells) express surface molecules that allow them to penetrate the blood–brain barrier and to enter the central nervous system (CNS). The presence of autoreactive immune effectors, together with abnormally activated CNS astrocytes and microglia, lead to increased production of reactive species, excitotoxicity, autoantibody production and direct cytotoxicity, which are all involved in demyelination, axonal and neuronal damage that is present in patients with MS. Potential therapeutic interventions at different levels of the immunopathological cascade are depicted in filled yellow boxes. CTL, cytotoxic T lymphocyte; IFN-, interferon-; IL, interleukin; IL2R, IL2 receptor; MHC II, major histocompatibility complex class II; MMPs, matrix metalloproteinases; NO, nitric oxide; ODG, oligodendrocyte; S1PR, sphingosine 1-phosphate receptor; TGF-, transforming growth factor-; TNF, tumour-necrosis factor; T_Reg cell, regulatory T cell; VCAM1, vascular cellular adhesion molecule 1; VLA4, very late antigen 4 (also known as ₄₁ integrin).

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