The ins and outs of T-lymphocyte trafficking to the CNS: anatomical sites and molecular mechanisms.

By B. Engelhardt, R. Ransohoff. Trends in immunology, 2005

678 citations recorded by the source corpus.

Subfields: Immunology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/f16c8028223ae02228fdd2480a32dea0f17fd300

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Citations in the corpus

The blood-brain barrier in Alzheimer's disease (2017, positive): “…increases strongly, and their soluble forms are released into the circulation to provide biomarkes of endothelial dysfunction and vascular in ﬂ ammation (Bö et al., 1996; Jander et al., 1996; Stins et al., 1997; Alvarez et al., 2011; Staykova et al., 2000; Garton et al., 2006; Rossi et al., 2011).”
Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδT cells (2016, neutral): “Some GFP + γδ T cell were also observed in the choroid plexus, a point of CNS entry for T cells 23 , while the brain parenchyma was devoid of γδ T cells (data not shown).”
BRAIN REGENERATION IN PHYSIOLOGY AND PATHOLOGY: THE IMMUNE SIGNATURE DRIVING THERAPEUTIC PLASTICITY OF NEURAL STEM CELLS (2011, background): “The concept of the CNS as an immune privileged site originates from studies showing that 1) foreign grafts are not strongly rejected in the brain; 2) there are no lymphatic vessels leaving the brain; 3) under normal conditions there are no infiltrating blood immune cells detectable in the CNS (67); ”
The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, positive): “…revealed at least three distinctive routes for leukocyte entry into the CNS: (1) from blood to CSF across the choroid plexus; (2) from blood to subarachnoid space; and (3) from blood to parenchymal perivascular space (Ransohoff et al., 2003; Engelhardt and Ransohoff, 2005; Man et al., 2007).”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “As a second step, autoreactive T cells, present in the normal immune repertoire, must be activated and acquire the capacity to migrate across the BBB (Engelhardt and Ransohoff, 2005).”
The blood–brain and the blood–cerebrospinal fluid barriers: function and dysfunction (2009, background): “This α4β1-integrin-mediated firm arrest to the inflamed BBB depends on heterotrimeric G(i)-linked receptors [74]; however, the chemokines and chemokine receptors mediating leukocyte integrin activation—a prerequisite for firm adhesion—at the BBB are not well defined [ 75 ].”
Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood (2006, background): “It is possible that the relevant T cells, which continuously survey the healthy CNS (refs”
C-C chemokine receptor 6–regulated entry of TH-17 cells into the CNS through the choroid plexus is required for the initiation of EAE (2009, background): “In contrast, the molecular requirements for lymphocyte rolling and adhesion to activated vessels of the inflamed blood-brain barrier have been intensively investigated in both active and passive models of EA”
The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “Because immunosurveillance exists in the CNS under physiological conditions with infiltration of activated leukocytes (essentially T lymphocytes and monocytes) across the cerebral endothelium, the former conception that the CNS was an immune privileged site has been recently tempered [91].”