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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;

/persons/resource/persons39114

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

/persons/resource/persons38946

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

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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: https://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.