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  Treg cells mediate recovery from EAE by controlling effector T cell proliferation and motility in the CNS

Koutrolos, M., Berer, K., Kawakami, N., Wekerle, H., & Krishnamoorthy, G. (2014). Treg cells mediate recovery from EAE by controlling effector T cell proliferation and motility in the CNS. Acta Neuropathologica Communications, 2: 163. doi:10.1186/s40478-014-0163-1.

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 Urheber:
Koutrolos, Michail1, Autor           
Berer, Kerstin1, Autor           
Kawakami, Naoto1, Autor           
Wekerle, Hartmut1, Autor           
Krishnamoorthy, Gurumoorthy1, Autor           
Affiliations:
1Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society, ou_1113547              

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Schlagwörter: Regulatory T cells, 2-photon imaging, Experimental autoimmune encephalomyelitis
 Zusammenfassung: Regulatory T cells are crucial in controlling various functions of effector T cells during experimental autoimmune
encephalomyelitis. While regulatory T cells are reported to exert their immunomodulatory effects in the peripheral
immune organs, their role within the central nervous system (CNS) during experimental autoimmune
encephalomyelitis is unclear. Here, by combining a selectively timed regulatory T cells depletion with 2-photon
microscopy, we report that regulatory T cells exercise their dynamic control over effector T cells in the CNS. Acute
depletion of regulatory T cells exacerbated experimental aut
oimmune encephalomyelitis sev
erity which was accompanied
by increased pro-inflammatory cytokine production and prolifer
ation of effector T cells. Intravital microscopy revealed that,
in the absence of regulatory T cells, the velocity of effector T cells was decreased with simultaneous increase in
the proportion of stationary phase cells in the CNS. Based on these data, we conclude that regulatory T cells mediate
recovery from experimental autoimmune encephalomyelitis by controlling cytokine production, proliferation and
motility of effector T cells in the CNS.

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Sprache(n): eng - English
 Datum: 2014-12-05
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: DOI: 10.1186/s40478-014-0163-1
 Art des Abschluß: -

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Titel: Acta Neuropathologica Communications
  Alternativer Titel : Acta Neuropathol Commun
Genre der Quelle: Zeitschrift
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Affiliations:
Ort, Verlag, Ausgabe: London : Biomed Central
Seiten: - Band / Heft: 2 Artikelnummer: 163 Start- / Endseite: - Identifikator: ISSN: 2051-5960