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

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Koutrolos,  Michail
Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Berer,  Kerstin
Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Kawakami,  Naoto
Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Wekerle,  Hartmut
Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Krishnamoorthy,  Gurumoorthy
Emeritus Group: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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40478_2014_Article_163.pdf
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Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0026-A213-5
Abstract
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.