Therapeutic developments for autoimmune demyelinating diseases: Musings from an MD (mouse doctor)

[1]  Yuhong Yang,et al.  MicroRNAs targeting TGFβ signalling underlie the regulatory T cell defect in multiple sclerosis. , 2016, Brain : a journal of neurology.

[2]  R. Elashoff,et al.  Estriol combined with glatiramer acetate for women with relapsing-remitting multiple sclerosis: a randomised, placebo-controlled, phase 2 trial , 2016, The Lancet Neurology.

[3]  D. Arnold,et al.  High-dose immunosuppressive therapy and autologous hematopoietic cell transplantation for relapsing-remitting multiple sclerosis (HALT-MS): a 3-year interim report. , 2015, JAMA neurology.

[4]  M. Racke,et al.  Is no evidence of disease activity a realistic goal for patients with multiple sclerosis? , 2015, JAMA neurology.

[5]  S. Lawler,et al.  Micro-RNA dysregulation in multiple sclerosis favours pro-inflammatory T-cell-mediated autoimmunity. , 2011, Brain : a journal of neurology.

[6]  Martin Röcken,et al.  Fumarates improve psoriasis and multiple sclerosis by inducing type II dendritic cells , 2012 .

[7]  E. Frohman,et al.  Multiple sclerosis--the plaque and its pathogenesis. , 2006, The New England journal of medicine.

[8]  A. Lovett-racke,et al.  Silencing T-bet defines a critical role in the differentiation of autoreactive T lymphocytes. , 2004, Immunity.

[9]  Nitin J. Karandikar,et al.  High prevalence of autoreactive, neuroantigen-specific CD8+ T cells in multiple sclerosis revealed by novel flow cytometric assay. , 2004, Blood.

[10]  A. Lovett-racke,et al.  Peroxisome Proliferator-Activated Receptor α Agonists as Therapy for Autoimmune Disease1 , 2004, The Journal of Immunology.

[11]  A. Lovett-racke,et al.  Peroxisome Proliferator-Activated Receptor-γ Agonist 15-Deoxy-Δ12,1412,14-Prostaglandin J2 Ameliorates Experimental Autoimmune Encephalomyelitis1 , 2002, The Journal of Immunology.

[12]  Nitin J. Karandikar,et al.  Glatiramer acetate (Copaxone) therapy induces CD8(+) T cell responses in patients with multiple sclerosis. , 2002, The Journal of clinical investigation.

[13]  A. Cross,et al.  T cells are the main cell type expressing B7‐1 and B7‐2 in the central nervous system during acute, relapsing and chronic experimental autoimmune encephalomyelitis , 1999, European journal of immunology.

[14]  P. Calabresi,et al.  Phase 1 trial of transforming growth factor beta 2 in chronic progressive MS , 1998, Neurology.

[15]  C. June,et al.  Decreased dependence of myelin basic protein-reactive T cells on CD28-mediated costimulation in multiple sclerosis patients. A marker of activated/memory T cells. , 1998 .

[16]  U. Utz,et al.  Longitudinal study of myelin basic protein-specific T-cell receptors during the course of multiple sclerosis , 1997, Journal of Neuroimmunology.

[17]  C. June,et al.  CTLA-4 blockade enhances clinical disease and cytokine production during experimental allergic encephalomyelitis. , 1996, Journal of immunology.

[18]  P. Albert,et al.  Role of B7:CD28/CTLA-4 in the induction of chronic relapsing experimental allergic encephalomyelitis. , 1995, Journal of immunology.

[19]  E. Shevach,et al.  Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease. , 1994 .

[20]  Roland Martin,et al.  Copolymer-1-induced inhibition of antigen-specific T cell activation: interference with antigen presentation , 1992, Journal of Neuroimmunology.

[21]  P. Albert,et al.  Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1. , 1991, Journal of immunology.