期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 1, 页码 30-34出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903412
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资金
- National Institutes of Health [P01 AI35297, R01 AI64677, U19 AI56388]
- Howard Hughes Medical Institute
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI056388, R01AI064677, P01AI035297, F32AI077199] Funding Source: NIH RePORTER
The possibility that effector T cells can be converted into forkhead box P3(+) regulatory T cells (Tregs) has potential therapeutic implications. To analyze the relationship between Th1 effectors and Tregs, we have used a model of systemic autoimmunity in which both effector and Tregs a-rise from a single population specific for a transgene-encoded systemic protein. In vitro, the presence of IFN-gamma inhibits Treg generation during activation. Using IFN-gamma reporter mice, we demonstrate that IFN-gamma-producing cells tend not to develop into Tregs, and Th1 priming of T cells prior to cell transfer limits the number of forkhead box P3(+) T cells generated in vivo. Moreover, transfer of IFN-gamma(-/-) or STAT1(-/-) T As resulted in an increase in the number of Tregs. These data support a role for Th1 effector molecules and transcription factors in the control of peripheral Treg generation and demonstrates the limited plasticity of Th1 populations. The Journal of Immunology, 2010, 184: 30-34.
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