title: Bioenergetics profile of CD4(+) T cells in relapsing remitting multiple sclerosis subjects.
abstract: Multiple sclerosis (MS) is a chronic inflammatory autoimmune demyelinating disease of the central nervous system. There are four clinical forms of MS, the most common of which is characterized by a relapsing remitting course (RRMS). The etiology of MS is unknown, but many studies suggested that genetic, environmental and infectious agents may contribute to the development of this disease. In experimental autoimmune encephalomyelitis (EAE), the animal model for MS, it has been shown that CD4(+) T cells play a key role in MS pathogenesis. In fact, these cells are able to cross the blood-brain barrier and cause axonal damage with neuronal death. T cell activation critically depends on mitochondrial ATP synthesis and reactive oxygen species (ROS) production. Interestingly, lots of studies linked the oxidative damage arising from mitochondrial changes to neurodegenerative disorders, such as MS. Based on these evidences, this work focused on the metabolic reprogramming of CD4(+) T cells in MS subjects, being this cell population directly implicated in pathogenesis of disease, paying attention to mitochondrial function and response to oxidative stress. Such aspects, once clarified, may open new opportunities for a therapeutic metabolic modulation of MS disorder.
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Lidia
authors.initials: L
authors.lastname: De Riccardis
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Antonia
authors.initials: A
authors.lastname: Rizzello
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Ferramosca
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Emanuela
authors.initials: E
authors.lastname: Urso
authors.affiliation: Department of Neurology, "Vito Fazzi" Hospital, ASL-Lecce, Italy.
authors.forename: Francesca
authors.initials: F
authors.lastname: De Robertis
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Danieli
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Giudetti
authors.affiliation: Department of Neurology, "Vito Fazzi" Hospital, ASL-Lecce, Italy.
authors.forename: Giorgio
authors.initials: G
authors.lastname: Trianni
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Zara
authors.affiliation: Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy. Electronic address: michele.maffia@unisalento.it.
authors.forename: Michele
authors.initials: M
authors.lastname: Maffia
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000201:enzymology / Q000473:pathology; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D010088:Oxidoreductases / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D055815:Young Adult
chemical_list: D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D010088:Oxidoreductases
keywords: CD4(+) T cells; Glycolysis; Multiple sclerosis; OXPHOS; Oxidative stress