Localizing central nervous system immune surveillance: Meningeal antigen‐presenting cells activate T cells during experimental autoimmune encephalomyelitis

The onset of neurological signs in experimental autoimmune encephalomyelitis is tightly associated with infiltration and reactivation of T cells in the central nervous system. The anatomic localization of the initial T cell‐antigen‐presenting cell (APC) interactions leading to reactivation of T cells in the central nervous system is, however, still unclear. We hypothesized that activated CD4+ T cells gain direct access to the subarachnoid space and become reactivated on encounter with cognate antigen in this compartment.

[1]  Hans Lassmann,et al.  Multiple sclerosis and Alzheimer's disease , 2008, Annals of neurology.

[2]  R. Reynolds,et al.  Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain , 2007, The Journal of experimental medicine.

[3]  P. Sawchenko,et al.  Time course and distribution of inflammatory and neurodegenerative events suggest structural bases for the pathogenesis of experimental autoimmune encephalomyelitis , 2007, The Journal of comparative neurology.

[4]  Hans Lassmann,et al.  Remyelination is extensive in a subset of multiple sclerosis patients. , 2006, Brain : a journal of neurology.

[5]  S. Cepok,et al.  Immune surveillance in multiple sclerosis patients treated with natalizumab , 2006, Annals of neurology.

[6]  R. Ransohoff,et al.  The many roles of chemokines and chemokine receptors in inflammation. , 2006, The New England journal of medicine.

[7]  R. Fujinami,et al.  Multiple sclerosis and virus induced immune responses: Autoimmunity can be primed by molecular mimicry and augmented by bystander activation , 2006, Autoimmunity.

[8]  N. Huang,et al.  B Cells Productively Engage Soluble Antigen-Pulsed Dendritic Cells: Visualization of Live-Cell Dynamics of B Cell-Dendritic Cell Interactions , 2005, The Journal of Immunology.

[9]  V. Kuchroo,et al.  The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity , 2005, Nature Immunology.

[10]  Britta Engelhardt,et al.  The circumventricular organs participate in the immunopathogenesis of experimental autoimmune encephalomyelitis , 2005, Cerebrospinal Fluid Research.

[11]  B. Engelhardt,et al.  The ins and outs of T-lymphocyte trafficking to the CNS: anatomical sites and molecular mechanisms. , 2005, Trends in immunology.

[12]  Tobias Bonhoeffer,et al.  Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion , 2005, The Journal of experimental medicine.

[13]  L. Steinman,et al.  Multiple sclerosis: trapped in deadly glue , 2005, Nature Medicine.

[14]  S. Miller,et al.  Epitope spreading initiates in the CNS in two mouse models of multiple sclerosis , 2005, Nature Medicine.

[15]  B. Becher,et al.  Dendritic cells permit immune invasion of the CNS in an animal model of multiple sclerosis , 2005, Nature Medicine.

[16]  B. Becher,et al.  Experimental autoimmune encephalomyelitis repressed by microglial paralysis , 2005, Nature Medicine.

[17]  B. Serafini,et al.  Detection of Ectopic B‐cell Follicles with Germinal Centers in the Meninges of Patients with Secondary Progressive Multiple Sclerosis , 2004, Brain pathology.

[18]  E. Baba,et al.  Three-dimensional two-layer collagen matrix gel culture model for evaluating complex biological functions of monocyte-derived dendritic cells. , 2004, Journal of immunological methods.

[19]  R. Ransohoff,et al.  The Activation Status of Neuroantigen-specific T Cells in the Target Organ Determines the Clinical Outcome of Autoimmune Encephalomyelitis , 2004, The Journal of experimental medicine.

[20]  S. Henrickson,et al.  T-cell priming by dendritic cells in lymph nodes occurs in three distinct phases , 2004, Nature.

[21]  P. McMenamin,et al.  Macrophages and dendritic cells in the rat meninges and choroid plexus: three-dimensional localisation by environmental scanning electron microscopy and confocal microscopy , 2003, Cell and Tissue Research.

[22]  R. Ransohoff,et al.  Three or more routes for leukocyte migration into the central nervous system , 2003, Nature Reviews Immunology.

[23]  R. Ransohoff,et al.  Recovery from EAE is associated with decreased survival of encephalitogenic T cells in the CNS of B7‐1/B7‐2‐deficient mice , 2003, European journal of immunology.

[24]  R. Ransohoff,et al.  Human cerebrospinal fluid central memory CD4+ T cells: Evidence for trafficking through choroid plexus and meninges via P-selectin , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[25]  H. Weiner,et al.  Myelin Oligodendrocyte Glycoprotein–specific T Cell Receptor Transgenic Mice Develop Spontaneous Autoimmune Optic Neuritis , 2003, The Journal of experimental medicine.

[26]  Sabine Stoll,et al.  Imaging of T‐cell interactions with antigen presenting cells in culture and in intact lymphoid tissue , 2002, Immunological reviews.

[27]  Michael Loran Dustin,et al.  T Cell Receptor Signaling Precedes Immunological Synapse Formation , 2002, Science.

[28]  Eugene C. Butcher,et al.  Molecular Mechanisms Involved in Lymphocyte Recruitment in Inflamed Brain Microvessels: Critical Roles for P-Selectin Glycoprotein Ligand-1 and Heterotrimeric Gi-Linked Receptors1 , 2002, The Journal of Immunology.

[29]  P. Popovich,et al.  Alterations in immune cell phenotype and function after experimental spinal cord injury. , 2001, Journal of neurotrauma.

[30]  B. Trapp,et al.  Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions , 2001, Annals of neurology.

[31]  S. Khoury,et al.  CD28-independent induction of experimental autoimmune encephalomyelitis. , 2001, The Journal of clinical investigation.

[32]  E. Bröcker,et al.  Antigen presentation in extracellular matrix: interactions of T cells with dendritic cells are dynamic, short lived, and sequential. , 2000, Immunity.

[33]  C. Janeway,et al.  Differential adhesion molecule requirements for immune surveillance and inflammatory recruitment. , 2000, Brain : a journal of neurology.

[34]  W. Hickey,et al.  Leukocyte traffic in the central nervous system: the participants and their roles. , 1999, Seminars in immunology.

[35]  C. Granger,et al.  Cerebrospinal fluid abnormalities in a phase III trial of Avonex® (IFNβ-1a) for relapsing multiple sclerosis 1 Studies supported by the National Multiple Sclerosis Society (grants RG2019, RG2827); the NINDS (NS26321); and Biogen Inc. 1 , 1999, Journal of Neuroimmunology.

[36]  P. Rakić,et al.  Changes in cell-cycle kinetics during the development and evolution of primate neocortex. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[37]  C. Gibbs,et al.  The 14-3-3 brain protein in cerebrospinal fluid as a marker for transmissible spongiform encephalopathies. , 1996, The New England journal of medicine.

[38]  B. Engelhardt,et al.  Lymphocyte Targeting of the Central Nervous System: A Review of Afferent and Efferent CNS‐Immune Pathways , 1996, Brain pathology.

[39]  L. Picker,et al.  Lymphocyte Homing and Homeostasis , 1996, Science.

[40]  S. Younkin,et al.  Amyloid β protein levels in cerebrospinal fluid are elevated in early‐onset Alzheimer's disease , 1994 .

[41]  S. Harik Cerebrospinal Fluid in Diseases of the Nervous System, 2nd Ed. , 1994, Neurology.

[42]  M. Sofroniew,et al.  Serum Proteins Bypass the Blood-Brain Fluid Barriers for Extracellular Entry to the Central Nervous System , 1993, Experimental Neurology.

[43]  R. Fishman Cerebrospinal Fluid in Diseases of the Nervous System , 1992 .

[44]  W. Hickey Migration of Hematogenous Cells Through the Blood‐Brain Barrier and the Initiation of CNS Inflammation , 1991, Brain pathology.

[45]  C. Brosnan,et al.  Homing to central nervous system vasculature by antigen-specific lymphocytes. I. Localization of 14C-labeled cells during acute, chronic, and relapsing experimental allergic encephalomyelitis. , 1990, Laboratory investigation; a journal of technical methods and pathology.

[46]  W. Hickey,et al.  Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo. , 1988, Science.

[47]  H. Wiśniewski,et al.  Chronic relapsing EAE time course of neurological symptoms and pathology , 1978, Acta Neuropathologica.

[48]  R. Adams,et al.  A histologic study of the early lesion in experimental allergic encephalomyelitis in the guinea pig and rabbit. , 1962, The American journal of pathology.

[49]  R. Reynolds,et al.  Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. , 2007, Brain : a journal of neurology.

[50]  C. Granger,et al.  Cerebrospinal fluid abnormalities in a phase III trial of Avonex (IFNbeta-1a) for relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group. , 1999, Journal of neuroimmunology.

[51]  S. Younkin,et al.  Amyloid beta protein levels in cerebrospinal fluid are elevated in early-onset Alzheimer's disease. , 1994, Annals of Neurology.

[52]  P. Knopf,et al.  Cervical lymphatics, the blood-brain barrier and the immunoreactivity of the brain: a new view. , 1992, Immunology today.