Journal
NATURE IMMUNOLOGY
Volume 10, Issue 9, Pages 1000-U104Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1774
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Funding
- US National Institutes of Health [P01 AI35297, U19 AI056388, P30 DK63720]
- American Diabetes Association
- Swiss National Science Foundation [PBBSB-118644]
- Roche Research Foundation
- Novartis Foundation
- US National Institute of General Medical Sciences [1 R25 GM56847]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI035297, U19AI056388, R37AI046643] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK063720, R00DK080885] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R25GM056847] Funding Source: NIH RePORTER
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Regulatory T cells (T-reg cells) are central to the maintenance of immune homeostasis. However, little is known about the stability of T-reg cells in vivo. In this study, we demonstrate that a substantial percentage of cells had transient or unstable expression of the transcription factor Foxp3. These 'exFoxp3' T cells had an activated-memory T cell phenotype and produced inflammatory cytokines. Moreover, exFoxp3 cell numbers were higher in inflamed tissues in autoimmune conditions. Adoptive transfer of autoreactive exFoxp3 cells led to the rapid onset of diabetes. Finally, analysis of the T cell receptor repertoire suggested that exFoxp3 cells developed from both natural and adaptive T-reg cells. Thus, the generation of potentially autoreactive effector T cells as a consequence of Foxp3 instability has important implications for understanding autoimmune disease pathogenesis.
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