Journal
CURRENT OPINION IN IMMUNOLOGY
Volume 21, Issue 6, Pages 612-618Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2009.09.011
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Funding
- Juvenile Diabetes Research Foundation International [1-2004-141, 3-2009-594]
- The Robert and Janice Compton Research [1-2006-847]
- NIH [A1072239]
- St Jude Cancer Center Support CORE [CA-21765]
- American Lebanese Syrian Associated Charities (ALSAC)
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Foxp3(+) regulatory T cells (T-regs) contribute significantly to the maintenance of peripheral tolerance, but they ultimately fail in autoimmune diseases. The events that lead to T-reg failure in controlling autoreactive effector T cells (T-effs,) during autoimmunity are not completely understood. In this review, we discuss possible mechanisms for this subversion as they relate to type 1 diabetes (T1D) and multiple sclerosis (MS). Recent studies emphasize firstly, the role of inflammatory cytokines, such as IL-6, in inhibiting or subverting T,g function; secondly, the issue of T-reg plasticity; thirdly, the possible resistance of autoimmune T cells to T-reg-mediated control; and fourthly, T-reg-associated inhibitory cytokines TGF beta, IL-10 and IL-35 in facilitating T-reg suppressive activity and promoting T-reg generation. These recent advances place a large emphasis on the local tissue specific inflammatory environment as it relates to T-reg function and disease development.
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