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VIP Prevents Experimental Multiple Sclerosis by Downregulating Both Inflammatory and Autoimmune Components of the Disease
Author(s) -
FERNANDEZMARTIN AMELIA,
GONZALEZREY ELENA,
CHORNY ALEJO,
MARTIN JAVIER,
POZO DAVID,
GANEA DOINA,
DELGADO MARIO
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1317.026
Subject(s) - multiple sclerosis , experimental autoimmune encephalomyelitis , neuropathology , vasoactive intestinal peptide , medicine , immunology , pathogenesis , autoimmune disease , inflammation , disease , myelin oligodendrocyte glycoprotein , autoimmunity , central nervous system , encephalomyelitis , neuroimmunology , immune system , pathology , receptor , neuropeptide , antibody
Multiple sclerosis (MS) is a disabling inflammatory, autoimmune demyelinating disease of the central nervous system (CNS). Despite intensive investigation, the mechanisms of disease pathogenesis remain unclear, and curative therapies are unavailable for MS. The current study describes a new possible strategy for the treatment of MS, based on the administration of the vasoactive intestinal peptide (VIP). Treatment with VIP significantly reduced incidence and severity of experimental autoimmune encephalomyelitis (EAE), an MS‐related rodent model. VIP suppressed EAE neuropathology by reducing CNS inflammation and by selective blocking encephalitogenic T‐cell reactivity, emerging as an attractive candidate for the treatment of human MS.