Premium
Plasmodium yoelii infection of BALB/c mice results in expansion rather than induction of CD4 + Foxp3 + regulatory T cells
Author(s) -
Abel Simone,
Ueffing Kristina,
Tatura Roman,
Hutzler Marina,
Hose Matthias,
Matuschewski Kai,
Kehrmann Jan,
Westendorf Astrid M.,
Buer Jan,
Hansen Wiebke
Publication year - 2016
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12602
Subject(s) - plasmodium yoelii , foxp3 , biology , immune system , regulatory t cell , immunology , il 2 receptor , microbiology and biotechnology , t cell , plasmodium falciparum , parasitemia , malaria
Summary 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 V β 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.