Cited by 248Multiple Sclerosis Research StudiesT-cell and B-cell ImmunologyNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.

Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion

Open access
Kawakami, Naoto, Nägerl, U. Valentin, Odoardi, Francesca, Bonhoeffer, Tobias, Wekerle, Hartmut, Flügel, Alexander·2005·The Journal of Experimental Medicine

Abstract

We tracked pathogenic myelin basic protein-specific CD4+ effector T cells in early central nervous system (CNS) lesions of experimental autoimmune encephalomyelitis (EAE) by combining two-photon imaging and fluorescence video microscopy. We made two key observations: (a) the majority of the cells (65%) moved fast (maximal speed 25 μm/min) and apparently nondirected through the compact tissue; and (b) a second group of effector T cells (35%) appeared tethered to a fixed point. Polarization of T cell receptor and adhesion molecules (lymphocyte function-associated antigen 1) towards this fixed point suggests the formation of immune synapses. Nonpathogenic, ovalbumin-specific T cells were not tethered in the CNS and did not form synapse-like contacts, but moved through the tissue. After intrathecal injection of antigen, 40% of ovalbumin-specific T cells became tethered. Conversely, injection of anti–major histocompatibility complex class II antibodies profoundly reduced the number of stationary pathogenic T cells within the CNS (to 15%). We propose that rapid penetration of the CNS parenchyma by numerous autoimmune effector T cells along with multiple autoantigen-presentation events are responsible for the fulminate development of clinical EAE.

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  • Activated T cells can enter the perivascular space independent of antigen specificity, but are unable to traverse the astrocytic basement membrane and glia limitans.

    “Activated T cells can enter the perivascular space independent of antigen specificity (82), but are unable to traverse the astrocytic basement membrane and glia limitans.”

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Research works printed but not linked: 3

  1. 2004, Immunity., 21, 315
  2. 1993, Am. J. Pathol., 143, 446
  3. 1979, Methods Enzymol., 32B, 323

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Metadata

Authors
Kawakami, N., Nägerl, U. V., Odoardi, F., Bonhoeffer, T., Wekerle, H., & Flügel, A.
Affiliations
  • Max Planck Institute of Neurobiology (DE)
  • 2Department of Cellular and Systems Neurobiology, Max-Planck-Institute of Neurobiology, 82152 Martinsried, Germany
  • 1Department of Neuroimmunology, Max-Planck-Institute of Neurobiology, 82152 Martinsried, Germany
Venue
The Journal of Experimental Medicine
Published
2005-06-06
Volume
201
Issue
11
Pages
1805-1814
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2153979851
Cited by
248
References
25
Citations by year
2026: 5 · 2025: 3 · 2024: 6 · 2023: 9 · 2022: 9 · 2021: 7 · 2020: 5 · 2019: 7 · 2018: 7 · 2017: 4 · 2016: 17 · 2015: 3 · 2014: 19 · 2013: 11 · 2012: 12
FWCI
15.92
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
  • Max Planck Digital Library (submittedVersion)
  • MPG.PuRe (Max Planck Society) (submittedVersion)
Funders
Deutsche Forschungsgemeinschaft (SFB455)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
experimental autoimmune encephalomyelitis, myelin basic protein, CD4+ T cells, autoantigen recognition, immunological synapse, CD11a/CD18, ovalbumin-specific T cells, MHC class II, autoantigen presentation, two-photon imaging
MeSH terms
Animals, Histocompatibility Antigens Class II, Autoantigens, Cell Communication, Cell Movement, Central Nervous System, Myelin Basic Protein, Encephalomyelitis, Autoimmune, Experimental, Guinea Pigs, Rats, Inbred Lew, Receptors, Antigen, T-Cell, CD4-Positive T-Lymphocytes, Lymphocyte Function-Associated Antigen-1, Antigen Presentation, Microscopy, Video, Microscopy, Fluorescence, Multiphoton, Rats

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