Soluble CD40 ligand disrupts the blood–brain barrier and exacerbates inflammation in experimental autoimmune encephalomyelitis

[1]  G. DeLuca,et al.  Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier , 2017, Journal of Neurology, Neurosurgery, and Psychiatry.

[2]  M. Mori,et al.  Soluble CD40 ligand contributes to blood–brain barrier breakdown and central nervous system inflammation in multiple sclerosis and neuromyelitis optica spectrum disorder , 2017, Journal of Neuroimmunology.

[3]  D. Fuchs,et al.  Blood–brain barrier integrity, intrathecal immunoactivation, and neuronal injury in HIV , 2016, Neurology: Neuroimmunology & Neuroinflammation.

[4]  Shota Suzuki Functional characterization of a new clone of conditionally immortalized human brain microvascular endothelial cells, HBMEC/ci18 , 2016 .

[5]  A. Lawson,et al.  CDP7657, an anti-CD40L antibody lacking an Fc domain, inhibits CD40L-dependent immune responses without thrombotic complications: an in vivo study , 2015, Arthritis Research & Therapy.

[6]  Daniel S. Reich,et al.  Direct MRI detection of impending plaque development in multiple sclerosis , 2015, Neurology: Neuroimmunology & Neuroinflammation.

[7]  F. Kurschus T cell mediated pathogenesis in EAE: Molecular mechanisms , 2015, Biomedical journal.

[8]  Y. Richard,et al.  The Signaling Role of CD40 Ligand in Platelet Biology and in Platelet Component Transfusion , 2014, International journal of molecular sciences.

[9]  H. Hartung,et al.  Immune regulation of multiple sclerosis. , 2014, Handbook of clinical neurology.

[10]  K. Kasischke,et al.  Excess Soluble CD40L Contributes to Blood Brain Barrier Permeability In Vivo: Implications for HIV-Associated Neurocognitive Disorders , 2012, PloS one.

[11]  Kosuke Saito,et al.  Establishment of a new conditionally immortalized cell line from human brain microvascular endothelial cells: A promising tool for human blood–brain barrier studies , 2012, Brain Research.

[12]  V. V. Agashe,et al.  Unique B cell responses in B cell-dependent and B cell-independent EAE , 2012, Autoimmunity.

[13]  Kaan E. Biron,et al.  Blood–brain barrier disruption and enhanced vascular permeability in the multiple sclerosis model EAE , 2010, Journal of Neuroimmunology.

[14]  L. Del Valle,et al.  Dyad of CD40/CD40 Ligand Fosters Neuroinflammation at the Blood–Brain Barrier and Is Regulated via JNK Signaling: Implications for HIV-1 Encephalitis , 2010, The Journal of Neuroscience.

[15]  R. Noelle,et al.  Molecular mechanism and function of CD40/CD40L engagement in the immune system , 2009, Immunological reviews.

[16]  N. Schmitz,et al.  CD40–CD40L cross-talk integrates strong antigenic signals and microbial stimuli to induce development of IL-17-producing CD4+ T cells , 2009, Proceedings of the National Academy of Sciences.

[17]  K. Stokes,et al.  CD40/CD40 Ligand Signaling in Mouse Cerebral Microvasculature After Focal Ischemia/Reperfusion , 2005, Circulation.

[18]  G. Becker Which albumin should we measure? , 2004, Kidney international. Supplement.

[19]  D. Boumpas,et al.  Lessons learned from anti-CD40L treatment in systemic lupus erythematosus patients , 2004, Lupus.

[20]  Michael J. Ramsbottom,et al.  Critical role of antigen‐specific antibody in experimental autoimmune encephalomyelitis induced by recombinant myelin oligodendrocyte glycoprotein , 2002, European journal of immunology.

[21]  A. Cross,et al.  B cells are critical to induction of experimental allergic encephalomyelitis by protein but not by a short encephalitogenic peptide , 1999, European journal of immunology.

[22]  R. Vakkalanka,et al.  Elevated levels and functional capacity of soluble CD40 ligand in systemic lupus erythematosus sera. , 1999, Arthritis and rheumatism.

[23]  J. Bonnefoy,et al.  Human Native Soluble CD40L Is a Biologically Active Trimer, Processed Inside Microsomes (*) , 1996, The Journal of Biological Chemistry.

[24]  R. K. Bergman,et al.  Vascular permeability changes in the central nervous system of rats with hyperacute experimental allergic encephalomyelitis induced with the aid of a substance from Bordetella pertussis , 1978, Infection and immunity.