title: Treg cells mediate recovery from EAE by controlling effector T cell proliferation and motility in the CNS.
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 autoimmune encephalomyelitis severity which was accompanied by increased pro-inflammatory cytokine production and proliferation 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.
authors.affiliation: Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152, Martinsried, Germany. koutrolos@neuro.mpg.de.
authors.forename: Michail
authors.initials: M
authors.lastname: Koutrolos
authors.affiliation: Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152, Martinsried, Germany. berer@neuro.mpg.de.
authors.forename: Kerstin
authors.initials: K
authors.lastname: Berer
authors.affiliation: Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152, Martinsried, Germany. kawakami@neuro.mpg.de.|Institute of Clinical Neuroimmunology, Ludwig-Maximilians-University, Marchioninistr. 15, 81377, Munich, Germany. kawakami@neuro.mpg.de.
authors.forename: Naoto
authors.initials: N
authors.lastname: Kawakami
authors.affiliation: Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152, Martinsried, Germany. hwekerle@neuro.mpg.de.
authors.forename: Hartmut
authors.initials: H
authors.lastname: Wekerle
authors.affiliation: Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152, Martinsried, Germany. guru@neuro.mpg.de.
authors.forename: Gurumoorthy
authors.initials: G
authors.lastname: Krishnamoorthy
mesh_terms: D000818:Animals; D002465:Cell Movement / Q000502:physiology*; D049109:Cell Proliferation / Q000502:physiology*; D002469:Cell Separation; D016207:Cytokines / Q000378:metabolism; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D007376:Interleukin-2 / Q000378:metabolism; D008810:Mice, Inbred C57BL; D012720:Severity of Illness Index; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology*; D050378:T-Lymphocytes, Regulatory / Q000502:physiology*
chemical_list: D016207:Cytokines; D007376:Interleukin-2