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  T cells become licensed in the lung to enter the central nervous system

Odoardi, F., Sie, C., Streyl, K., Ulaganathan, V. K., Schlaeger, C., Lodygin, D., et al. (2012). T cells become licensed in the lung to enter the central nervous system. Nature, 488(7413), 675-679. doi:10.1038/nature11337.

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© 2012 Nature Publishing Group
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 Urheber:
Odoardi, Francesca, Autor           
Sie, Christopher, Autor
Streyl, Kristina, Autor           
Ulaganathan, Vijay Kumar, Autor           
Schlaeger, Christian, Autor
Lodygin, Dmitri, Autor
Heckelsmiller, Klaus, Autor           
Nietfeld, Wilfried1, Autor           
Ellwart, Joachim, Autor
Klinkert, Wolfgang E. F., Autor           
Lottaz, Claudio, Autor
Nosov, Mikhail, Autor           
Brinkmann, Volker, Autor           
Spang, Rainer, Autor           
Lehrach, Hans1, Autor           
Vingron, Martin2, Autor           
Wekerle, Hartmut, Autor           
Fluegel-Koch, Cassandra, Autor
Fluegel, Alexander, Autor
Affiliations:
1Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1433550              
2Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1479639              

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Schlagwörter: EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; ADHESION MOLECULE; MICROARRAY DATA; MYELOID CELLS; LYMPHOCYTES; MIGRATION; ANTIGEN; CNS; INFECTIONS
 Zusammenfassung: The blood–brain barrier (BBB) and the environment of the central nervous system (CNS) guard the nervous tissue from peripheral immune cells. In the autoimmune disease multiple sclerosis, myelin-reactive T-cell blasts are thought to transgress the BBB1, 2 and create a pro-inflammatory environment in the CNS, thereby making possible a second autoimmune attack that starts from the leptomeningeal vessels and progresses into the parenchyma3, 4, 5, 6. Using a Lewis rat model of experimental autoimmune encephalomyelitis, we show here that contrary to the expectations of this concept, T-cell blasts do not efficiently enter the CNS and are not required to prepare the BBB for immune-cell recruitment. Instead, intravenously transferred T-cell blasts gain the capacity to enter the CNS after residing transiently within the lung tissues. Inside the lung tissues, they move along and within the airways to bronchus-associated lymphoid tissues and lung-draining mediastinal lymph nodes before they enter the blood circulation from where they reach the CNS. Effector T cells transferred directly into the airways showed a similar migratory pattern and retained their full pathogenicity. On their way the T cells fundamentally reprogrammed their gene-expression profile, characterized by downregulation of their activation program and upregulation of cellular locomotion molecules together with chemokine and adhesion receptors. The adhesion receptors include ninjurin 1, which participates in T-cell intravascular crawling on cerebral blood vessels. We detected that the lung constitutes a niche not only for activated T cells but also for resting myelin-reactive memory T cells. After local stimulation in the lung, these cells strongly proliferate and, after assuming migratory properties, enter the CNS and induce paralytic disease. The lung could therefore contribute to the activation of potentially autoaggressive T cells and their transition to a migratory mode as a prerequisite to entering their target tissues and inducing autoimmune disease.

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Sprache(n): eng - English
 Datum: 2012-08-222012-08-30
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1038/nature11337
 Art des Abschluß: -

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Titel: Nature
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: London : Nature Publishing Group
Seiten: - Band / Heft: 488 (7413) Artikelnummer: - Start- / Endseite: 675 - 679 Identifikator: ISSN: 0028-0836
CoNE: https://pure.mpg.de/cone/journals/resource/954925427238