期刊
JOURNAL OF IMMUNOLOGY
卷 203, 期 2, 页码 370-378出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1900388
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- Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI000959] Funding Source: NIH RePORTER
The transcription factor Helios is expressed in a large percentage of Foxp3(+) regulatory T (Treg) cells and is required for the maintenance of their suppressive phenotype, as mice with a selective deficiency of Helios in Treg cells spontaneously develop autoimmunity. However, mice with a deficiency of Helios in all T cells do not exhibit autoimmunity, despite the defect in the suppressor function of their Treg cell population, suggesting that Helios also functions in non-Treg cells. Although Helios is expressed in a small subset of CD4(+)Foxp3(-) and CD8(+)T cells and its expression is upregulated upon T cell activation, its function in non-Treg cells remains unknown. To examine the function of Helios in CD4(+)Foxp3(-)T cells, we transferred Helios-sufficient or -deficient naive CD4(+) Foxp3(-) TCR transgenic T cells to normal recipients and examined their capacity to respond to their cognate Ag. Surprisingly, Helios-deficient CD4(+)T cells expanded and differentiated into Th1 or Th2 cytokine-producing effectors in a manner similar to wild-type TCR transgenic CD4(+)T cells. However, the primed Helios-deficient cells failed to expand upon secondary challenge with Ag. The tolerant state of the Helios-deficient memory T cells was not cell-intrinsic but was due to a small population of Helios-deficient naive T cells that had differentiated into Ag-specific peripheral Treg cells that suppressed the recall response in an Ag-specific manner. These findings demonstrate that Helios plays a role in the determination of CD4(+)T cell fate.
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