Table 1.
Forms | Disease mechanism |
---|---|
Relapsing MS | Relapsing MS is driven by immune cells that migrate to CNS. Currently there are a variety of treatments by intervention of these pathways reduce the recurrence of MS: reducing the number/function of effector cells, increasing the number/ function of regulating cells, preventing cells from being transported to the CNS |
Progressive MS | The immune response in the central nervous system is dominant in the progressive stage, as well as immune independent is included. A micro-environment is created within the CNS favoring homing and retention of inflammatory cells (B cells, pro-inflammatory cytokines), causing disease-modifying therapies to ineffective |
ADEM | Two hypotheses for the pathogenic of ADEM: The molecular mimicry and The postinfectious etiology hypothesis. The changes of immune system during pregnancy will inevitably lead to changes in cytokine levels. Plasma exchange may remove harmful circulating antibodies that can alleviate clinical symptoms |
NMOSD | The peripheral circulation contains auto-antibodies against aquaporin-4 (AQP4-IgG). AQP4-IgG enter to the CNS across the BBB cause a series of pathological changes. Maternal placenta can expression of AQP 4, leading to AQP 4 antibody-mediated placental attack, may also be a causative factor |
MS, multiple sclerosis; ADEM, Acute disseminated encephalomyelitis; NMOSD, Neuromyelitis optica spectrum disorders; AQP4, anti-aquaporin-4; CNS, central nervous system.