• Makoto Miyara, Yoshinaga Ito, and Shimon Sakaguchi.
• Department of Immunology, Department of Internal Medicine, Pitié-Salpêtrière Hospital, APHP, 83 Boulevard de l'Hôpital, 75013 Paris, France.
• Nat Rev Rheumatol. 2014 Sep 1;10(9):543-51.

AbstractNaturally occurring Foxp3(+)CD25(+)CD4(+) regulatory T (TREG) cells maintain immunological self-tolerance and prevent a variety of autoimmune diseases, including rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus. In animal models of rheumatic disease, autoimmune responses can be controlled by re-establishing the T-cell balance in favour of TREG cells. Here we discuss three potential strategies for the clinical use of TREG cells to treat autoimmune rheumatic disease: expansion of self-antigen-specific natural TREG cells in vivo; propagation of antigen-specific natural TREG cells ex vivo, by in vitro antigenic stimulation, and subsequent transfer back into the host; or conversion of antigen-specific conventional T cells into TREG cells in vivo or ex vivo. These strategies require depletion of the effector T cells that mediate autoimmunity before initiating TREG-cell-based therapies. Immunotherapies that target TREG cells, and the balance of TREG cells and autoreactive T cells, are therefore an important modality for the treatment of autoimmune rheumatic disease.

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