Journal
IMMUNITY
Volume 30, Issue 1, Pages 80-91Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2008.11.010
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Funding
- National Institutes of Health
- European Union through MUGEN
- Ministry of Education, Culture, Sports, Science, and Technology of Japan
- Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation
- Leukemia and Lymphoma Society
- Portuguese Foundation for Science and Technology
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Foxp3(+) regulatory T (Treg) cells limit pathogenic immune responses to self-antigens and foreign antigens. An essential role for microRNA (miRNA) in the maintenance and function of Treg cells, revealed by the Treg cell-specific Dicer ablation, raised a question as to a specific miRNA contribution. We found that Foxp3 controlled the elevated miR155 expression required for maintaining Treg cell proliferative activity and numbers under nonlymphopenic conditions. Moreover, miR155 deficiency in Treg cells resulted in increased suppressor of cytokine signaling 1 (SOCS1) expression accompanied by impaired activation of signal transducer and activator of transcription 5 (STAT5) transcription factor in response to limiting amounts of interleukin-2. Our studies suggest that Foxp3-dependent regulation of miR155 maintains competitive fitness of Treg cells by targeting SOCS1, and they provide experimental support for a proposed role for miRNAs in ensuring the robustness of cellular phenotypes.
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