Myelin Damage in MS

Another critical determinant in the cascade of events leading to MS lesion development is antigen presentation. Antigen presenting cell (APC)/T-cell activation involves at least four major processes (1) Molecular mi mi cry, (2) Epitope spreading, (3) Bystander activation, and (4) Cryptic antigen 

Bystander activation activation of autoreactive cells through nonspecific inflammation and induction of inflammatory cytokines and chemokines is also of pathological consequence in MS. It has been suggested that bystander activation, induced by persistent virus infection or primed by molecular mimicry may activate autoreactive T-cells specific for the CNS (McCoy et al., 2006). Einally, cryptic antigens may also play a role in immune activation. In other immune-mediated diseases such as Chronic Lymphocytic Thyroiditis and Chagas Heart Disease, exposure of cryptic epitopes leads to the activation of autoimmune cells and further contributes to 

Peripheral immune aystem (lymph nodes, spleen, blood) 

Specific C04+ T cede Initiate myelin damage by various effector mechanisms production of cytokines and chemoklnes activation of macrophagesy microglia production of reactive oxygen species and nitric oxide CDS T cells and B cells also participate as effectors 

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