The unwavering commitment of regulatory T cells in the suppression of autoimmune encephalomyelitis: Another aspect of immune privilege in the CNS

Authors

  • Benjamin M. Segal

    Corresponding author
    1. Holtom-Garrett Program in Neuroimmunology,, Department of Neurology, University of Michigan, Ann Arbor, MI, USA
    • Full correspondence:Dr. Benjamin M. Segal, Holtom-Garrett Program in Neuroimmunology, 4013 BSRB, 109 Zina Pitcher Place, SPC 2200, Ann Arbor, MI 48109, USA

      Fax: +1-734-615-7300

      e-mail: bmsegal@umich.edu

      See accompanying article: http://dx.doi.org/10.1002/eji.201142216

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  • See accompanying article by O'Connor et al.

Abstract

FoxP3+ regulatory T (Treg) cells accumulate in the central nervous system (CNS) during experimental autoimmune encephalomyelitis and have been shown to limit the extent of neuroinflammation and to facilitate clinical recovery. The recent demonstration that Treg cells lose FoxP3 expression and assume effector cell characteristics upon stimulation with proinflammatory cytokines has raised questions about their stability in the inflamed CNS. In this issue of the European Journal of Immunology, O'Connor et al. [Eur. J. Immunol. 2012. 42: 1164–1173] show that CNS-infiltrating Treg cells maintain their suppressor phenotype by downregulating the IL-6 receptor. This commentary discusses the finding particularly with relevance to therapy of multiple sclerosis.

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