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  • Print publication year: 2009
  • Online publication date: July 2016

Chapter 4 - Negotiating the brain barriers:

from Section 1: - Interactions between the immune and nervous systems

References

Abbott NJ, et al. Astrocyte–endothelial interactions at the blood–brain barrier. Nat Rev Neurosci 2006; 7: 41–53.
Adamson P, et al. Lymphocyte migration through brain endothelial cell monolayers involves signaling through endothelial ICAM-1 via a rho-dependent pathway. J Immunol 1999; 162: 2964–73.
Allt G, Lawrenson JG. Is the pial microvessel a good model for blood–brain barrier studies? Brain Res Brain Res Rev 1997; 24: 67–76.
Alt C, et al. Functional expression of the lymphoid chemokines CCL19 (ELClc) and CCL21 (SLC) at the blood–brain barrier suggests their possible involvement in lymphocyte recruitment into the central nervous system during experimental autoimmune encephalomyelitis. Eur J Immunol 2002; 32: 2133–44.
Andras IE, et al. Signaling mechanisms of HIV-1 Tat-induced alterations of claudin-5 expression in brain endothelial cells. J Cereb Blood Flow Metab 2005; 25: 1159–70.
Archelos JJ, et al. Inhibition of experimental autoimmune encephalomyelitis by an antibody to the intercellular adhesion molecule ICAM-1. Ann Neurol 1993; 34: 145–54.
Banks WA, et al. The blood–brain barrier in neuroaids. Curr HIV Res 2006; 4: 259–66.
Barragan A, Sibley LD. Migration of Toxoplasma gondii across biological barriers. Trends Microbiol 2003; 11: 426–30.
Barragan A, et al. Transepithelial migration of Toxoplasma gondii involves an interaction of intercellular adhesion molecule 1 (ICAM-1) with the parasite adhesin MIC2. Cell Microbiol 2005; 7: 561–8.
Barreiro O, et al. Dynamic interaction of VCAM-1 and ICAM-1 with moesin and ezrin in a novel endothelial docking structure for adherent leukocytes. J Cell Biol 2002; 157: 1233–45.
Battistini L, et al. Cd8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: A critical role for P-selectin glycoprotein ligand-1. Blood 2003; 101: 4775–82.
Betz LA, et al. Blood brain–cerebrospinal fluid barriers. In Siegel GJ (Ed.), Basic Neurochemistry: Molecular, Cellular, And Medical Aspects. New York: Raven Press.
Bo L, et al. Distribution of immunoglobulin superfamily members ICAM-1, -2, -3, and the beta 2 integrin LFA-1 in multiple sclerosis lesions. J Neuropathol Exp Neurol 1996; 55: 1060–72.
Bouchaud C, Bosler O. The circumventricular organs of the mammalian brain with special reference to monoaminergic innervation. Int Rev Cytol 1986; 105: 283–327.
Brocke S, et al. Antibodies to Cd44 and integrin alpha4, but not L-selectin, prevent central nervous system inflammation and experimental encephalomyelitis by blocking secondary leukocyte recruitment. Proc Natl Acad Sci USA 1999; 96: 6896–901.
Bullard DC, et al. Intercellular adhesion molecule-1 expression is required on multiple cell types for the development of experimental autoimmune encephalomyelitis. J Immunol 2007; 178: 851–7.
Butcher EC, et al. Lymphocyte trafficking and regional immunity. Adv Immunol 1999; 72: 209–53.
Cannella B, et al. Anti-adhesion molecule therapy in experimental autoimmune encephalomyelitis. J Neuroimmunol 1993; 46: 43–55.
Carlos TM, Harlan JM. Leukocyte–endothelial adhesion molecules. Blood 1994; 7: 2068–101.
Carman CV, Springer TA. A transmigratory cup in leukocyte diapedesis both through individual vascular endothelial cells and between them. J Cell Biol 2004; 167: 377–88.
Carrithers MD, et al. Differential adhesion molecule requirements for immune surveillance and inflammatory recruitment. Brain 2000; 123: 1092–101.
Carrithers MD, et al. Role of genetic background in P Selectin-dependent immune surveillance of the central nervous system. J Neuroimmunol 2002; 129: 51–7.
Carvalho-Tavares J, et al. A role for platelets and endothelial selectins in tumor necrosis factor-alpha-induced leukocyte recruitment in the brain microvasculature. Circ Res 2000; 87: 1141–8.
Cattelino A, et al. The conditional inactivation of the {beta}-catenin gene in endothelial cells causes a defective vascular pattern and increased vascular fragility. J Cell Biol 2003; 162: 1111–22.
Columba-Cabezas S, et al. Lymphoid chemokines CCL19 And CCL21 are expressed in the central nervous system during experimental autoimmune encephalomyelitis: Implications for the maintenance of chronic neuroinflammation. Brain Pathol 2003; 13: 38–51.
Courret N, et al. Cd11c- and Cd11b-expressing mouse leukocytes transport single Toxoplasma gondii tachyzoites to the brain. Blood 2006; 107: 309–16.
Crone C, Olesen SP. Electrical resistance of brain microvascular endothelium. Brain Res 1982; 241: 49–55.
Cross AH, Raine CS. Central nervous system endothelial cell–polymorphonuclear cell interactions during autoimmune demyelination. Am J Pathol 1991; 139: 1401–9.
Deckert Schluter M, et al. Differential expression of ICAM-1, VCAM-1 and their ligands LFA-1, MAC-1, CD43, VLA-4, and MHC class II antigens in murine toxoplasma encephalitis: A light microscopic and ultrastructural immunohistochemical study. J Neuropathol Exp Neurol 1994; 53: 457–68.
Del Maschio A, et al. Leukocyte recruitment in the cerebrospinal fluid of mice with experimental meningitis is inhibited by an antibody to junctional adhesion molecule (JAM). J Exp Med 1999; 190: 1351–6.
Doulet N, et al. Neisseria meningitidis infection of human endothelial cells interferes with leukocyte transmigration by preventing the formation of endothelial docking structures. J Cell Biol 2006; 173: 627–37.
Dzenko KA, et al. The chemokine receptor Ccr2 mediates the binding and internalization of monocyte chemoattractant protein-1 along brain microvessels. J Neurosci 2001; 21: 9214–23.
Dziegielewska KM, et al. Development of the choroid plexus. Microsc Res Tech 2001; 52: 5–20.
Ebnet K, et al. Junctional adhesion molecules (JAMs): More molecules with dual functions? J Cell Sci 2004; 117: 19–29.
Engelhardt B. Development of the blood–brain barrier. Cell Tissue Res 2003; 314: 119–29.
Engelhardt B, Ransohoff RM. The ins and outs of T-lymphocyte trafficking to the CNS: Anatomical sites and molecular mechanisms. Trends Immunol 2005; 26: 485–95.
Engelhardt B, Wolburg H. Mini-review: Transendothelial migration of leukocytes – Through the front door or around the side of the house? Eur J Immunol 2004; 34: 2955–63.
Engelhardt B, et al. Lymphocytes infiltrating the CNS during inflammation display a distinctive phenotype and bind to VCAM-1 but not to MADCAM-1. Int Immunol 1995; 7: 481–91.
Engelhardt B, et al. E- and P-selectin are not involved in the recruitment of inflammatory cells across the blood–brain barrier in experimental autoimmune encephalomyelitis. Blood 1997; 90: 4459–72.
Engelhardt B, et al. The development of experimental autoimmune encephalomyelitis in the mouse requires alpha4-integrin but not alpha4beta7-integrin. J Clin Invest 1998a; 102: 2096–105.
Engelhardt B, et al. Adhesion molecule phenotype of T lymphocytes in inflamed CNS. J Neuroimmunol 1998b; 84: 92–104.
Engelhardt B, et al. Involvement of the choroid plexus in central nervous system inflammation. Microsc Res Tech 2001; 52: 112–29.
Engelhardt B, et al. PSGL-1 is not required for the development of experimental autoimmune encephalomyelitis in SJL and C57bl6 mice. J Immunol 2005; 175: 1267–75.
Graesser D, et al. Altered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1-deficient mice. J Clin Invest 2002; 109: 383–92.
Greenwood J, et al. Intracellular domain of brain endothelial intercellular adhesion molecule-1 is essential for T lymphocyte-mediated signaling and migration. J Immunol 2003; 171: 2099–108.
Grewal IS, et al. Cd62l is required on effector cells for local interactions in the CNS to cause myelin damage in experimental allergic encephalomyelitis. Immunity 2001; 14: 291–302.
Hickey WF, et al. T-lymphocyte entry into the central nervous system. J Neurosci Res 1991; 28: 254–60.
Huang S, Jong AY. Cellular mechanisms of microbial proteins contributing to invasion of the blood–brain barrier. Cell Microbiol 2001; 3: 277–87.
Johnson AK, Gross PM. Sensory circumventricular organs and brain homeostatic pathways. FASEB J 2003; 7: 678–86.
Johnson-Léger C, Imhof BA. Forging the endothelium during inflammation: Pushing at a half-open door? Cell Tiss Res 2003; 314: 93–105.
Kanmogne GD, et al. HIV-1 Gp120 compromises blood–brain barrier integrity and enhances monocyte migration across blood–brain barrier: Implication for viral neuropathogenesis. J Cereb Blood Flow Metab 2007; 27: 123–34.
Kent SJ, et al. A monoclonal antibody to alpha 4 integrin suppresses and reverses active experimental allergic encephalomyelitis. J Neuroimmunol 1995; 58: 1–10.
Kerfoot S, Kubes P. Overlapping roles of P-selectin and alpha 4 integrin to recruit leukocytes to the central nervous system in experimental autoimmune encephalomyelitis. J. Immunol 2002; 169: 1000–6.
Kim KS. Microbial translocation of the blood–brain barrier. Int J Parasitol 2006; 36: 607–14.
Kivisakk P, et al. Human cerebrospinal fluid central memory CD4+ T cells: Evidence for trafficking through choroid plexus and meninges via P-selectin. Proc Natl Acad Sci USA 2005; 100: 8389–94. Epub 2003 Jun 26.
Kleine TO, Benes L. Immune surveillance of the human central nervous system (CNS): Different migration pathways of immune cells through the blood–brain barrier and blood–cerebrospinal fluid barrier in healthy persons. Cytometry A 2006; 69: 147–51.
Laschinger M, Engelhardt, B. Interaction of alpha4-integrin with VCAM-1 is involved in adhesion of encephalitogenic T cell blasts to brain endothelium but not in their transendothelial migration in vitro. J Neuroimmunol 2000; 102: 32–43.
Laschinger M, et al. Encephalitogenic T cells use LFA-1 during transendothelial migration but not during capture and adhesion in spinal cord microvessels in vivo. Eur J Immunol 2002; 32: 3598–606.
Lechner F, et al. Antibodies to the junctional adhesion molecule cause disruption of endothelial cells and do not prevent leukocyte influx into the meninges after viral or bacterial infection. J Infect Dis 2000; 182: 978–82.
Leonhardt H. Ependym und Circumventriculäre Organe. In Oksche A, Vollrath L (Eds.), Handbuch der Mikroskopischen Anatomie des Menschen. Berlin/Heidelberg/New York: Springer, 1980a.
Leonhardt H. Ependym und Zirkumventrikuläre Organe. Berlin: Springer, 1980b.
Luster AD, et al. Immune cell migration in inflammation: Present and future therapeutic targets. Nat Immunol 2005; 6: 1182–90.
Lyck R, et al. T-cell interaction with ICAM-1/ICAM-2 double-deficient brain endothelium in vitro: The cytoplasmic tail of endothelial ICAM-1 is necessary for transendothelial migration of T cells. Blood 2003; 102: 3675–83.
Maclean AG, et al. Activation of the blood–brain barrier by SIV (simian immunodeficiency virus) requires cell-associated virus and is not restricted to endothelial cell activation. Biochem Soc Trans 2004; 32: 750–2.
Martin R, Mcfarland HF. Immunological aspects of experimental allergic encephalomyelitis and multiple sclerosis. Crit Rev Clin Lab Sci 1995; 32: 121–82.
Martin-Padura I, et al. Junctional adhesion molecule, a novel member of the immunoglobulin superfamily that distributes at intercellular junctions and modulates monocyte transmigration. J Cell Biol 1998; 142: 117–27.
Millan J, et al. Lymphocyte transcellular migration occurs through recruitment of endothelial ICAM-1 to caveola- and F-actin-rich domains. Nat Cell Biol 2006; 8: 113–23. Epub 2006 Jan 22.
Muller WA. Leukocyte–endothelial cell interactions in leukocyte transmigration and the inflammatory response. Trends Immunol 2003; 6: 327–34.
Nasdala I, et al. A transmembrane tight junction protein selectively expressed on endothelial cells and platelets. J Biol Chem 2002; 277: 16294–303.
Osmers I, et al. PSGL-1 is not required for development of experimental autoimmune encephalomyelitis. J Neuroimmunol 2005; 166: 193–6.
Padden M, et al. differences in expression of junctional adhesion molecule-A and beta-catenin in multiple sclerosis brain tissue: Increasing evidence for the role of tight junction pathology. Acta Neuropathol (Berl) 2007; 113: 177–86. Epub 2006 Oct 6.
Pardridge WM. Blood–brain barrier delivery. Drug Discov Today 2007; 12: 54–61.
Phillipson M, et al. Intraluminal crawling of neutrophils to emigration sites: A molecularly distinct process from adhesion in the recruitment cascade. J Exp Med 2006; 203: 2569–75.
Piccio L, et al. Efficient recruitment of lymphocytes in inflamed brain venules requires expression of cutaneous lymphocyte antigen and fucosyltransferase-VII. J Immunol 2005; 174: 5805–13.
Piccio L, et al. Molecular mechanisms involved in lymphocyte recruitment in inflamed brain microvessels: Critical roles for P-selectin glycoprotein ligand-1 and heterotrimeric G(I)-linked receptors. J Immunol 2002; 168: 1940–9.
Plumb J, et al. Abnormal endothelial tight junctions in active lesions and normal-appearing white matter in multiple sclerosis. Brain Pathol 2002; 12: 154–69.
Polman CH, et al. A randomized, placebo-controlled trial of Natalizumab for relapsing multiple sclerosis. N Engl J Med 2006; 354: 899–910.
Qing Z, et al. Inhibition of antigen-specific T cell trafficking into the central nervous system via blocking PECAM1/CD31 molecule. J Neuropathol Exp Neurol 2001; 60: 798–807.
Rascher G, Wolburg H. The tight junctions of the leptomeningeal blood–cerebrospinal fluid barrier during development. J Hirnforsch 1997; 38: 525–40.
Reiss Y, et al. T cell interaction with ICAM-1-deficient endothelium in vitro: Essential role for ICAM-1 and ICAM-2 in transendothelial migration of T cells. Eur J Immunol 1998; 28: 3086–99.
Ring A, et al. Pneumococcal trafficking across the blood–brain barrier. Molecular analysis of a novel bidirectional pathway. J Clin Invest 1998; 102: 347–60.
Risau W, et al. Immune function of the blood–brain barrier: Incomplete presentation of protein (auto-)antigens by rat brain microvascular endothelium in vitro. J Cell Biol 1990; 110: 1757–66.
Rudick RA, et al. Natalizumab plus interferon beta-1a for relapsing multiple sclerosis. N Engl J Med 2006; 354: 911–23.
Schluter D, et al. Immune reactions to Listeria monocytogenes in the brain. Immunobiology 1999; 201: 188–95.
Schulz M, Engelhardt B. The circumventricular organs participate in the immunopathogenesis of experimental autoimmune encephalomyelitis. Cerebrospinal Fluid Res 2005; 2: 8.
Schulze C, Firth JA. Immunohistochemical localization of adherens junction components in blood–brain barrier microvessels of the rat. JCell Sci 1993; 104: 773–82.
Sedgwick JD, et al. Antigen-specific damage to brain vascular endothelial cells mediated by encephalitogenic and nonencephalitogenic CD4+ T cell lines in vitro. J Immunol 1990; 145: 2474–81.
Sixt M, et al. Endothelial cell laminin isoforms, laminins 8 and 10, play decisive roles in T cell recruitment across the blood–brain barrier in experimental autoimmune encephalomyelitis. J Cell Biol 2001; 153: 933–46.
Sobel RA, et al. Intercellular adhesion molecule-1 (ICAM-1) in cellular immune reactions in the human central nervous system. Am J Pathol 1990; 136: 1309–16.
Steffen BJ, et al. ICAM-1, VCAM-1, and MADCAM-1 are expressed on choroid plexus epithelium but not endothelium and mediate binding of lymphocytes in vitro. Am J Pathol 1996; 148: 1819–38.
Steffen BJ, et al. Evidence for involvement of ICAM-1 and VCAM-1 in lymphocyte interaction with endothelium in experimental autoimmune encephalomyelitis in the central nervous system in the SJL/J mouse. Am J Pathol 1994; 145: 189–201.
Ubogu EE, et al. The expression and function of chemokines involved in CNS inflammation. Trends Pharmacol Sci 2006; 27: 48–55.
Vajkoczy P, et al. Alpha4-integrin-VCAM-1 binding mediates G protein-independent capture of encephalitogenic T cell blasts to CNS white matter microvessels. J Clin Invest 2001; 108: 557–65.
Wekerle H, et al. Cellular immune reactivity within the CNS. TINS 1986; 9: 271–7.
Welsh CT, et al. Augmentation of adoptively transferred experimental allergic encephalomyelitis by administration of a monoclonal antibody specific for LFA-1a. J Neuroimmunol 1993; 43: 161–8.
Willenborg DO, et al. ICAM-1-dependent pathway is not critically involved in the inflammatory process of autoimmune encephalomyelitis or in cytokine-induced inflammation of the central nervous system. J Neuroimmunol 1993; 45: 147–54.
Wolburg H, Lippoldt A. Tight junctions of the blood–brain barrier. Development, composition and regulation. Vasc Pharmacol 2002; 28: 323–37.
Wolburg H, et al. Localization of claudin-3 in tight junctions of the blood–brain barrier is selectively lost during experimental autoimmune encephalomyelitis and human glioblastoma multiforme. Acta Neuropathol (Berl) 2003; 105: 586–92.
Wolburg H, et al. Osp/claudin-11, claudin-1 and claudin-2 are present in tight junctions of choroid plexus epithelium of the mouse. Neurosci Lett 2001; 13: 77–80.
Yednock TA, et al. Prevention of experimental autoimmune encephalomyelitis by antibodies against alpha 4 beta 1 integrin. Nature 1992; 356: 63–6.
Yousry TA, et al. Evaluation of patients treated with Natalizumab for progressive multifocal leukoencephalopathy. N Engl J Med 2006; 354: 924–33.
Zeine R, Owens T. Direct demonstration of the infiltration of murine central nervous system by PGP-1/Cd44 high Cd45rblow Cd4+ T cells that induce experimental allergic encephalomyelitis. J Neuroimmunol 1992; 40: 57–70.