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Modulation of the Immune Response is Skin Deep
Author(s) -
Bynoe Margaret S.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1074.5
Subject(s) - experimental autoimmune encephalomyelitis , multiple sclerosis , immunology , myelin oligodendrocyte glycoprotein , immune system , central nervous system , oligodendrocyte , immunization , encephalomyelitis , medicine , myelin , biology , neuroscience
Multiple sclerosis (MS) is an inflammatory attack on the central nervous system (CNS) that results in extensive demyelination and loss of neuronal function that often leads to death. Experimental autoimmune encephalomyelitis (EAE) is the animal model for MS. We have recently observed that when we epicutaneously immunize (on shaved skin) C57BL/6 mice with the autoantigen myelin oligodendrocyte gylcpprotein (MOG), in a skin patch prior to inducing EAE with MOG that these mice are protected from developing EAE. Most importantly, when we epicutaneously immunize mice with MOG after they develop EAE, mice with mild EAE are protected, but not mice with severe EAE. We observed that CD4 T cells from mice that are protected from EAE produced high levels of IL‐10 and they can transfer protection to naïve recipient mice. We also found that epidermal dendritic cells that captured antigen from the patch can suppress EAE when they are isolated after epicutaneous immunization and transferred into naïve recipient mice. These studies will serve to advance our knowledge of autoimmune disease regulation both at the peripheral level and at the CNS level and could be beneficial to MS and other autoimmune diseases.