Higher susceptibility to experimental autoimmune encephalomyelitis in Muc1-deficient mice is associated with increased Th1/Th17 responses.

ABSTRACT: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system in which dendritic cells (DC) play an important role in the development of inflammatory responses. Recently it has been shown that Muc1, a membrane tethered glycoprotein, has an ability to suppress inflammatory responses in cultured DC. The objective of this study was to investigate the possible involvement of Muc1 in the development of MS using experimental autoimmune encephalomyelitis (EAE) in mice, a widely used animal model of MS. Our results showed that: (1) Muc1(-/-) mice developed greater EAE severity compared with wild type (wt) mice, which correlated with increased numbers of Th1 and Th17 cells infiltrating into the CNS; (2) upon stimulation, splenic DC from Muc1(-/-) mice produced greater amounts of IL

SUBMITTER: Yen JH 

PROVIDER: S-EPMC3587144 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature