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Human regulatory T cells and their role in autoimmune disease

Authors

  • Clare Baecher-Allan,

    1. Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA, USA
    2. Harvard Medical School, Boston, MA, USA
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  • David A. Hafler

    Corresponding author
    1. Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA, USA
    2. Harvard Medical School, Boston, MA, USA
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David A Hafler, MD
Breakstone Professor of Neurology
Harvard Medical School
Brigham and Women's Hospital
Center for Neurologic Disease, NRB 641
77 Avenue Louis Pasteur
Boston
MA 021215
USA
Tel.: +1 617 525 5330
Fax: +1 617 525 5333
E-mail: dhafler@rics.bwh.harvard.edu

Abstract

Summary:  As self-recognition is fundamental to the efficient operation of the immune system, a number of mechanisms have evolved to keep this potential pathologic self-reactivity in check. Thus, even though the majority of strongly self-reactive T cells are deleted in the thymus during T-cell maturation, a number of mature T cells that recognize self-antigens can be found in the peripheral circulation in healthy individuals as well as in patients with autoimmune disease. These self-reactive cells are kept in a non-responsive state in healthy individuals while they appear to be involved in the etiology of a number of autoimmune diseases in patients. The primary role of a relatively recently identified T-cell population, referred to as natural CD4+CD25+ regulatory T cells, is to modulate the activity of these self-reactive cells. Although it is still unclear how these regulatory cells function, they can inhibit the activation of other potentially pathologic T cells in in vitro assays. Using such assays, regulatory T cells isolated from patients with a number of autoimmune diseases have been shown to exhibit reduced inhibitory function as compared with those isolated from healthy individuals. In this review, we discuss human natural regulatory T cells, what is known about their function, and their associations with specific autoimmune diseases.

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