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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis

Fig. 1

Pathological manifestations of peripheral immune cells in MS. The pathogenesis of MS goes through three main phases: the autoimmune response (A), the chronic inflammatory response (B), and the demyelinating reaction (C). During the autoimmune reaction stage (A), various immune cells, such as T cells, B cells, and myelin-specific CD4+ T cells, penetrate the brain tissue through the blood–brain barrier (BBB). In the chronic inflammatory response (B), adaptive Th cells, Treg, and B cells release cytokines or interferon-γ and antibodies to contribute to the inflammatory response. Additionally, innate immune macrophages (Mϕ), and natural killer (NK) cells secrete substances like histamine, trypsin, ROS, NO, inflammatory cytokines, and Granzyme B, which participate in the inflammatory response. Peripheral immune cells, particularly T cells, B cells, monocytes and Mϕ, contribute to the demyelination process in MS through direct interactions with oligodendrocytes, the release of pro-inflammatory molecules, and the production of antibodies against myelin proteins. MS monocytes inhibit the phagocytic capacity of myeline debris, whereas exosomes derived from DCs promote myelination (C)

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