Laquinimod interferes with migratory capacity of T cells and reduces IL-17 levels, inflammatory demyelination and acute axonal damage in mice with experimental autoimmune encephalomyelitis
暂无分享,去创建一个
C. Wegner | W. Brück | R. Alon | C. Stadelmann | B. Timan | L. Hayardeny | Sara W. Feigelson | E. Raymond | Ramona Pförtner
[1] B. Becher,et al. IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice. , 2008, The Journal of clinical investigation.
[2] B. Sun,et al. IL‐17 Eliminates the Therapeutic Effects of Myelin Basic Protein‐Induced Nasal Tolerance in Experimental Autoimmune Encephalomyelitis by Activating IL‐6 , 2008, Scandinavian journal of immunology.
[3] Hiroko Nakatsukasa,et al. Repeated 0.5-Gy γ Irradiation Attenuates Experimental Autoimmune Encephalomyelitis with Up-regulation of Regulatory T Cells and Suppression of IL17 Production , 2008, Radiation research.
[4] P. Tonali,et al. IL17 and IFNgamma production by peripheral blood mononuclear cells from clinically isolated syndrome to secondary progressive multiple sclerosis. , 2008, Cytokine.
[5] G. Comi,et al. Effect of laquinimod on MRI-monitored disease activity in patients with relapsing-remitting multiple sclerosis: a multicentre, randomised, double-blind, placebo-controlled phase IIb study , 2008, The Lancet.
[6] C. Teuscher,et al. IL-13-Mediated Gender Difference in Susceptibility to Autoimmune Encephalomyelitis1 , 2008, The Journal of Immunology.
[7] R. Alon,et al. DOCK2 regulates chemokine-triggered lateral lymphocyte motility but not transendothelial migration. , 2006, Blood.
[8] Hans Lassmann,et al. Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. , 2006, Brain : a journal of neurology.
[9] T. Leanderson,et al. Inhibition of the development of chronic experimental autoimmune encephalomyelitis by laquinimod (ABR-215062) in IFN-β k.o. and wild type mice , 2006, Journal of Neuroimmunology.
[10] L. Steinman,et al. Virtues and pitfalls of EAE for the development of therapies for multiple sclerosis. , 2005, Trends in immunology.
[11] F. Barkhof,et al. Treatment with laquinimod reduces development of active MRI lesions in relapsing MS , 2005, Neurology.
[12] G. Hedlund,et al. Laquinimod (ABR-215062) suppresses the development of experimental autoimmune encephalomyelitis, modulates the Th1/Th2 balance and induces the Th3 cytokine TGF-β in Lewis rats , 2004, Journal of Neuroimmunology.
[13] Wolfgang Brück,et al. Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time. , 2002, Brain : a journal of neurology.
[14] J. Kira,et al. Increased IL-13 but not IL-5 production by CD4-positive T cells and CD8-positive T cells in multiple sclerosis during relapse phase , 2002, Journal of the Neurological Sciences.
[15] G. Hedlund,et al. The new orally active immunoregulator laquinimod (ABR-215062) effectively inhibits development and relapses of experimental autoimmune encephalomyelitis , 2002, Journal of Neuroimmunology.
[16] B. Engelhardt,et al. Functional expression of the lymphoid chemokines CCL19 (ELC) and CCL 21 (SLC) at the blood‐brain barrier suggests their involvement in G‐protein‐dependent lymphocyte recruitment into the central nervous system during experimental autoimmune encephalomyelitis , 2002, European journal of immunology.
[17] B. Winblad,et al. Suppression of experimental autoimmune neuritis by ABR-215062 is associated with altered Th1/Th2 balance and inhibited migration of inflammatory cells into the peripheral nerve tissue , 2002, Neuropharmacology.
[18] B. Engelhardt,et al. Alpha4-integrin-VCAM-1 binding mediates G protein-independent capture of encephalitogenic T cell blasts to CNS white matter microvessels. , 2001, The Journal of clinical investigation.
[19] R. Rudick,et al. Neurological disability correlates with spinal cord axonal loss and reduced N‐acetyl aspartate in chronic multiple sclerosis patients , 2000, Annals of neurology.
[20] Amnon Peled,et al. Subsecond Induction of α4 Integrin Clustering by Immobilized Chemokines Stimulates Leukocyte Tethering and Rolling on Endothelial Vascular Cell Adhesion Molecule 1 under Flow Conditions , 2000, The Journal of experimental medicine.
[21] J. Wolinsky,et al. Linomide in relapsing and secondary progressive MS , 2000, Neurology.
[22] V. Oikonen,et al. Access www.neurology.org now for full-text articles , 2000, Neurology.
[23] Ganter,et al. Spinal cord axonal loss in multiple sclerosis: a post‐mortem study , 1999, Neuropathology and applied neurobiology.
[24] A. al‐Sabbagh,et al. Interferon beta modulates experimental autoimmune encephalomyelitis by altering the pattern of cytokine secretion. , 1999, Immunological investigations.
[25] B. Engelhardt,et al. The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. , 1998, The Journal of clinical investigation.
[26] R. Rudick,et al. Axonal transection in the lesions of multiple sclerosis. , 1998, The New England journal of medicine.
[27] Hans Lassmann,et al. Inflammatory central nervous system demyelination: Correlation of magnetic resonance imaging findings with lesion pathology , 1997, Annals of neurology.
[28] V. Perry,et al. Axonal damage in acute multiple sclerosis lesions. , 1997, Brain : a journal of neurology.
[29] M. Sela,et al. Copolymer 1 inhibits chronic relapsing experimental allergic encephalomyelitis induced by proteolipid protein (PLP) peptides in mice and interferes with PLP-specific T cell responses , 1996, Journal of Neuroimmunology.
[30] A. Ben-nun,et al. Inhibition of acute, experimental autoimmune encephalomyelitis by the synthetic immunomodulator linomide , 1993, Annals of neurology.
[31] D. Karussis,et al. Treatment of chronic-relapsing experimental autoimmune encephalomyelitis with the synthetic immunomodulator linomide (quinoline-3-carboxamide). , 1993, Proceedings of the National Academy of Sciences of the United States of America.