The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Molecular dissection of the miR-17-92 cluster's critical dual roles in promoting Th1 responses and preventing inducible Treg differentiation
Open accessAbstract
Mir-17-92 encodes 6 miRNAs inside a single polycistronic transcript, the proper expression of which is critical for early B-cell development and lymphocyte homeostasis. However, during the T-cell antigen response, the physiologic function of endogenous miR-17-92 and the roles of the individual miRNAs remain elusive. In the present study, we functionally dissected the miR-17-92 cluster and revealed that miR-17 and miR-19b are the key players controlling Th1 responses through multiple coordinated biologic processes. These include: promoting proliferation, protecting cells from activation-induced cell death, supporting IFN-γ production, and suppressing inducible regulatory T-cell differentiation. Mechanistically, we identified Pten (phosphatase and tensin homolog) as the functionally important target of miR-19b, whereas the function of miR-17 is mediated by TGFβRII and the novel target CREB1. Because of its vigorous control over the Th1 cell–inducible regulatory T cell balance, the loss of miR-17-92 in CD4 T cells results in tumor evasion. Our results suggest that miR-19b and miR-17 could be harnessed to enhance the efficacy of T cell–based tumor therapy.
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Metadata
- Authors
- Jiang, S., Li, C., Olive, V., Lykken, E., Feng, F., Sevilla, J., Wan, Y., He, L., & Li, Q.-J.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2011-11-17
- Volume
- 118
- Issue
- 20
- Pages
- 5487-5497
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1992015602
- Cited by
- 297
- References
- 45
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Jiang, S., Li, C., Olive, V., Lykken, E., Feng, F., Sevilla, J., Wan, Y., He, L., & Li, Q.-J. (2011). Molecular dissection of the miR-17-92 cluster's critical dual roles in promoting Th1 responses and preventing inducible Treg differentiation. Blood. https://doi.org/10.1182/blood-2011-05-355644
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