期刊
CLINICAL IMMUNOLOGY
卷 123, 期 1, 页码 18-29出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2006.10.014
关键词
regulatory T cells; FOXP3; human; CD4; CD8
类别
资金
- NIAID NIH HHS [R01 AI053439] Funding Source: Medline
CD4(+)CD25(+)FOXP3(+) regulatory T-cells (T-regs) form an important arm of the immune system responsible for suppressing untoward immune responses. T-regs can be thymically derived or peripherally induced, even from CD4(+)CD25(-)FOXP3(-) T-cells. FOXP3 expression and in vitro suppressive activity are considered unique hallmarks of this dedicated and stable lineage of regulatory cells. Here we show that virtually all human CD4(+)CD25(-)FOXP3(-) T-cells and CD8(+)CD25(-)FOXP3(-) T-cells attain a transient FOXP3(+)CD25(+) state during activation. In this state of activation, these cells possess the classic phenotype of T-regs, in that they express similar markers and inhibit in vitro proliferation of autologous CD4(+)CD25(-) T-cells. This state is characterized by suppressed IFN-gamma production and robust TNF-alpha and IL-10 production. Interestingly, the great majority of the activated cells eventually downregulate FOXP3 expression, with a concomitant drop in suppressive ability. Our results show that, in humans, FOXP3 expression and T-reg functionality are not exclusive features of a stable or unique lineage of T-cells but may also be a transient state attained by almost all T-cells. These results warrant caution in interpreting human studies using FOXP3 and suppressive activity as readouts and suggest that attempts to induce T-regs may paradoxically result in induction of effector T-cells, unless stability is confirmed. (c) 2006 Elsevier Inc. All rights reserved.
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