期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 5, 页码 2578-2582出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0803162
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- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C236, BB/E011659/1, BB/E009867/1, BBS/E/B/0000C206] Funding Source: researchfish
- Medical Research Council [G0601618, G0700287] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/E009867/1, BBS/E/B/0000C236, BB/E011659/1, BBS/E/B/0000C206] Funding Source: Medline
- Medical Research Council [G0601618, G0700287] Funding Source: Medline
- BBSRC [BB/E009867/1, BBS/E/B/0000C236, BB/E011659/1] Funding Source: UKRI
- MRC [G0700287, G0601618] Funding Source: UKRI
Foxp3 is a transcription factor that is essential for the normal development of regulatory T cells (Tregs). In the absence of microRNAs (miRNAs), Foxp3(+) Tregs develop but fail to maintain immune homeostasis, leading to a scurfy-like disease. Global analysis of the network of genes regulated by Foxp3 has identified the miRNA miR-155, which is highly expressed in Tregs, as a direct target of Foxp3. In this study we report that miR-155-deficient mice have reduced numbers of Tregs, both in the thymus and periphery, due to impaired development. However, we found no evidence for defective suppressor activity of miR-155-deficient Tregs, either in vitro or in vivo. Our results indicate that miR-155 contributes to Treg development, but that additional miRNAs control Treg function. The Journal of Immunology, 2009, 182: 2578-2582.
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