Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by destruction of the myelin sheath structure. The loss of myelin leads to damage of a neuron's axon and cell body, which is identified as brain lesions on magnetic resonance image (MRI). The pathogenesis of MS remains largely unknown. However, immune mechanisms, especially those linked to the aberrant lymphocyte activity, are mainly responsible for neuronal damage. Th1 and Th17 populations of lymphocytes were primarily associated with MS pathogenesis. These lymphocytes are essential for differentiation of encephalitogenic CD8(+) T cell and Th17 lymphocyte crossing the blood brain barrier and targeting myelin sheath in the CNS. B-lymphocytes could also contribute to MS pathogenesis by producing anti-myelin basic protein antibodies. In later studies, aberrant function of Treg and Th9 cells was identified as contributing to MS. This review summarizes the aberrant function and count of lymphocyte, and the contributions of these cell to the mechanisms of MS. Additionally, we have outlined the novel MS therapeutics aimed to amend the aberrant function or counts of these lymphocytes.

Automated summary

Multiple sclerosis is a chronic inflammatory disease of the central nervous system characterized by destruction of the myelin sheath. Immune mechanisms, particularly abnormal lymphocyte activity, play a key role in the pathogenesis of multiple sclerosis. This review summarizes the abnormal function and count of lymphocytes and their contributions to the mechanisms of multiple sclerosis. Additionally, novel therapies aimed at correcting the aberrant function or count of these lymphocytes are discussed.