Multiple Sclerosis (MS) is an autoimmune inflammatory disorder of the Central
Nervous System (CNS), affecting more than one million people worldwide. The
pathogenesis of MS involves several genetic and environmental factors, which
ultimately lead to the activation of autoreactive T cells in the periphery, their
migration into the CNS, where they trigger an acute inflammatory response,
thus mediating primary demyelination and axonal damage. Most information
on MS derives from studies in animal models of experimental autoimmune
encephalomyelitis (EAE), which exhibit many similarities to the pathology of
MS. Two distinct subsets of autoreactive T cells have been primarily involved in
the pathogenesis of both EAE and MS: the interferon (IFN)-γ producing CD4+ T
helper (Th) 1 and interleukin (IL)-17 producing Th17 cells. The activity of these
cells is controlled by specific regulatory T cells (Treg), which by secreting antiinflammatory
cytokines such as IL-4, IL-10 and tumour growth factor (TGF)-β
efficiently inhibit Th1 and Th17 cells.
In this review, we summarize current knowledge on the role and function of
pro-inflammatory and Treg subsets in MS. We also discuss the action of current
and novel therapies aimed to dampen inflammatory T cells