Inflammation and Oxidative Stress in Multiple Sclerosis: Consequences for Therapy Development

Table 1

Overview of the cellular immune contribution to MS pathology.

Cell	Effect	Role
B cells	Proinflammatory	Antibody production, antigen presentation to T cells, cytokine production; Participate in the adaptive immune response [25, 43, 45, 46]
CD4^+ T cells	Proinflammatory	Recognize and proliferate in response to autoantigens, cytokine production, drive the inflammatory process [22, 26]
CD8^+ T cells	Proinflammatory	Recognize and proliferate in response to foreign/self-antigens, target cell cytotoxicity, main T cell type present in MS lesions [24, 26, 32]
CNS dendritic cells	Proinflammatory	Involved in (re)presentation of MS autoantigens to active T cells [61–63]
Macrophage (M1)	Proinflammatory	Activated in response to T cell infiltration, phagocytosis, antigen presentation to T cells, production of proinflammatory cytokines, chemokines, and nitric oxide, increase neuropathy, represent the majority of macrophages in active MS [48, 66]
Macrophage (M2)	Anti-inflammatory	Phagocytosis, antigen presentation to T cells, production of anti-inflammatory cytokines, involved in repair mechanisms, low numbers found deep inside MS lesions [66]
Microglia	Both	CNS surveillance and host defense, activated in MS lesions, production of cytokines, roles in tissue damage and repair, but differential roles to infiltrating macrophages not well understood [48, 52, 56, 58, 67, 71]
T helper (Th17) cells	Proinflammatory	Significant initiator of inflammation in CNS [64]
Tregs	Anti-inflammatory	Suppress autoimmunity, low expression in MS brain tissue [37, 38, 41, 42]