1. Plasmodium yoelii infection of BALB/c mice results in expansion rather than induction of CD4(+) Foxp3(+) regulatory T cells.
- Author
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Abel S, Ueffing K, Tatura R, Hutzler M, Hose M, Matuschewski K, Kehrmann J, Westendorf AM, Buer J, and Hansen W
- Subjects
- Animals, Cell Differentiation, Cells, Cultured, DNA Methylation, Forkhead Transcription Factors genetics, Forkhead Transcription Factors metabolism, Humans, Mice, Mice, Inbred BALB C, Neuropilin-1 metabolism, Receptors, Antigen, T-Cell, alpha-beta genetics, Receptors, Antigen, T-Cell, alpha-beta metabolism, Cell Proliferation, Lymphocyte Activation, Malaria immunology, Plasmodium yoelii immunology, T-Lymphocytes, Regulatory immunology
- Abstract
Recently, we demonstrated elevated numbers of CD4(+) Foxp3(+) regulatory T (Treg) cells in Plasmodium yoelii-infected mice contributing to the regulation of anti-malarial immune response. However, it remains unclear whether this increase in Treg cells is due to thymus-derived Treg cell expansion or induction of Treg cells in the periphery. Here, we show that the frequency of Foxp3(+) Treg cells expressing neuropilin-1 (Nrp-1) decreased at early time-points during P. yoelii infection, whereas percentages of Helios(+) Foxp3(+) Treg cells remained unchanged. Both Foxp3(+) Nrp-1(+) and Foxp3(+) Nrp-1(-) Treg cells from P. yoelii-infected mice exhibited a similar T-cell receptor Vβ chain usage and methylation pattern in the Treg-specific demethylation region within the foxp3 locus. Strikingly, we did not observe induction of Foxp3 expression in Foxp3(-) T cells adoptively transferred to P. yoelii-infected mice. Hence, our results suggest that P. yoelii infection triggered expansion of naturally occurring Treg cells rather than de novo induction of Foxp3(+) Treg cells., (© 2016 John Wiley & Sons Ltd.)
- Published
- 2016
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