Journal
PLOS BIOLOGY
Volume 6, Issue 11, Pages 2401-2413Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pbio.0060276
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Funding
- Carlsberg Foundation
- Medical Research Council
- Arthritis Research Campaign [18297]
- MRC [MC_U105184296] Funding Source: UKRI
- Medical Research Council [MC_U105184296] Funding Source: researchfish
- Versus Arthritis [18297] Funding Source: researchfish
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Forkhead box p3 (Foxp3)-expressing regulatory T cells are key mediators of peripheral tolerance suppressing undesirable immune responses. Ectopic expression of Foxp3 confers regulatory T cell phenotype to conventional T cells, lending itself to therapeutic use in the prevention of autoimmunity and transplant rejection. Here, we show that adoptive transfer of polyclonal, wild-type T cells transduced with an inducible form of Foxp3 (iFoxp3) can be used to suppress immune responses on demand. In contrast to Foxp3-transduced cells, iFoxp3-transduced cells home correctly'' into secondary lymphoid organs, where they expand and participate in immune responses. Upon induction of iFoxp3, the cells assume regulatory T cell phenotype and start to suppress the response they initially partook in without causing systemic immunosuppression. We used this approach to suppress collagen-induced arthritis, in which conventional Foxp3-transduced cells failed to show any effect. This provides us with a generally applicable strategy to specifically halt immune responses on demand without prior knowledge of the antigens involved.
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