Role of the Programmed Death-1 (PD-1) pathway in regulation of Theiler's murine encephalomyelitis virus-induced demyelinating disease.

Programmed death-1 (PD-1) belongs to the CD28 family of co-stimulatory and co-inhibitory molecules and regulates adaptive immunity. This molecule induces the development of regulatory T cells, T cell tolerance, or apoptosis. We examined the role of PD-1 pathway in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) mice.

The TIM-3 pathway ameliorates Theiler's murine encephalomyelitis virus-induced demyelinating disease.

Infection by Theiler's murine encephalomyelitis virus (TMEV) in the central nervous system (CNS) induces an immune-mediated demyelinating disease in susceptible mouse strains and serves as a relevant infection model for human multiple sclerosis. T-cell immunoglobulin and mucin domain-3 (TIM-3) has been demonstrated to play a crucial role in the maintenance of peripheral tolerance. In this study, we examined the regulatory role of the TIM-3 pathway in the development of TMEV-induced demyelinating disease (TMEV-IDD).

Downregulation of water channel aquaporin-4 in rats with experimental autoimmune encephalomyeritis induced by myelin basic protein.

Characteristics of myelin basic protein (MBP)-induced experimental autoimmune encephalomyelitis (EAE) include acute edema and infiltration of mononuclear cells (MNCs) in the microvessels of central nervous system (CNS). Aquaporin-4 (AQP4) is a water channel protein expressed in astrocytes foot process throughout the CNS. We performed immunostaining, western blotting and semi-quantitative real-time RT-PCR of AQP4 and glial fibrillary acidic protein (GFAP) in CNS from rats immunized with MBP.

Therapeutic effects of anti-Delta1 mAb on Theiler's murine encephalomyelitis virus-induced demyelinating disease.

We examined the role of Notch ligand Delta-like 1 (Delta1) in the development of Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD). Blocking of Delta1 by anti-Delta1 monoclonal antibody (mAb) in the effector phase significantly suppressed the disease development of TMEV-IDD both clinically and histologically. The number of infiltrating inflammatory mononuclear cells in the spinal cords was also decreased in mice treated with anti-Delta1 mAb at the effector phase.