Figure 5.

cAMP, the possible crossroad between lymphocytes and mitochondrial dysfunctions in multiple sclerosis (MS). The figure shows the alterations of lymphocytes (blue semicircle) and mitochondrial lymphocytes (red semicircle) observed in MS. cyclic AMP (cAMP) level has been found decrease in peripheral blood mononuclear cells of relapsing remitting (RR) MS patients [84]. The general observation on T cells is that increasing cAMP levels, by phosphodiesyterase inhibitors (PDEi) [74,78,79,80] or by nutraceutics interventions [113], attenuates the T lymphocyte mediated immune response by decreasing the pro-inflammatory cytokines production (e.g., interferon-γ (IFN-γ), tumor necrosis α (TNF-α), and interleukin-1β), T cell proliferation, activation, and migration in central nervous system (CNS) as well as increases their apoptosis. Mitochondrial alterations have been observed in lymphocytes of MS in terms of mitochondrial respiration, coupling, dynamics, structure, biogenesis, and mitochondria-mediated apoptosis. Although cAMP is a master regulator of mitochondrial metabolism and structure [116], no information is available on mitochondrial rescues after increasing cAMP level in MS lymphocytes.