Treg and T-effector cells in autoimmune CNS inflammation: A delicate balance, easily disturbed

Authors

  • Stephen M. Anderton

    Corresponding author
    1. Medical Research Council/University of Edinburgh Centre for Inflammation Research, Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, Edinburgh, UK
    • Medical Research Council/University of Edinburgh Centre for Inflammation Research, Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK Fax: +44-131-242-6560
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Abstract

EAE is the primary pre-clinical disease for modelling the autoimmune/inflammatory component of multiple sclerosis. In fact, EAE is the primordial CD4+ T-cell-driven autoimmune disease model. It is striking (although perhaps unsurprising) that more than 10 000 publications over seven decades have provided a confusing, rather than a satisfying, picture of etiopathology. In the current issue of the European Journal of Immunology, an analysis of mice lacking LFA-1 is reported. Given the role of this integrin in T-cell activation and effector cell migration, one might predict resistance of LFA-1−/− mice to EAE induction. Instead, this study unexpectedly reports that EAE was exacerbated in the absence of LFA-1, and that this correlated with a decrease in the steady-state numbers of Foxp3+ Treg in the LFA-1−/− mice. Previous studies on the role of LFA-1 in EAE have been reviewed recently. This Commentary focuses on our current understanding of Treg function in the development and resolution of EAE and discusses how the absence of LFA-1 might unhinge these, possibly by altering the generation of Treg in the thymus, their expansion in response to autoantigen immunization, or their infiltration of the CNS.

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