title: Impact of mast cells on multiple sclerosis: inhibitory effect of natalizumab.
abstract: Mast cells (MCs) derive from a distinct precursor in the bone marrow and are predominantly found in tissues at the interface between the host and the external environment where they can secrete mediators without overt degranulation. Mast cells mature under local tissue microenvironmental factors and are necessary for the development of allergic reactions, through crosslinking of their surface receptors for IgE (FcεRI), leading to degranulation and the release of vasoactive, pro-inflammatory and nociceptive mediators that include histamine, pro-inflammatory and anti-inflammatory cytokines and proteolytic enzymes. Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demylination within the central nervous system. MCs are involved in the pathogenesis of MS by generating various vasoactive mediators and cytokines and participate in the destruction of the myelin sheath and the neuronal cells. The process of the development of demyelinating plaques in MS is probably linked with the rupture of the blood-brain barrier by MC products. The effects of natalizumab, which is a very effective drug in reducing the annualized relapse rate and other relapse-based endpoints, are discussed. Here, we report the relationship between MCs and MS.
authors.affiliation: Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.
authors.forename: S K
authors.initials: SK
authors.lastname: Kritas
authors.affiliation: Department of Dermatology, University of Rome Tor Vergata, Rome, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Saggini
authors.affiliation: Nicola's Foundation, Onlus, Arezzo, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Cerulli
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Caraffa
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Antinolfi
authors.affiliation: Orthopedic Division, University of Chieti-Pescara, Chieti, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Pantalone
authors.affiliation: Gynecology Clinic, Pescara Hospital, Pescara, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Rosati
authors.affiliation: Nicola's Foundation, Onlus, Arezzo, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Tei
authors.affiliation: Nicola's Foundation, Onlus, Arezzo, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Speziali
authors.affiliation: Department of Neurosciences and Imaging, Faculty of Medicine and Surgery, G. d'Annunzio University Chieti-Pescara, Chieti, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Saggini
authors.affiliation: Aristotle University of Thessaloniki, Macedonia, Greece.
authors.forename: A
authors.initials: A
authors.lastname: Frydas
authors.affiliation: Immunology Division, Medical School, University of Chieti-Pescara, Chieti, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Conti
mesh_terms: D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D006801:Humans; D039441:Integrin alpha4 / Q000276:immunology*; D008407:Mast Cells / Q000502:physiology*; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000209:etiology*; D000069442:Natalizumab
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D000069442:Natalizumab; D039441:Integrin alpha4