The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
miR-146a controls the resolution of T cell responses in mice
Open accessAbstract
T cell responses in mammals must be tightly regulated to both provide effective immune protection and avoid inflammation-induced pathology. NF-κB activation is a key signaling event induced by T cell receptor (TCR) stimulation. Dysregulation of NF-κB is associated with T cell–mediated inflammatory diseases and malignancies, highlighting the importance of negative feedback control of TCR-induced NF-κB activity. In this study we show that in mice, T cells lacking miR-146a are hyperactive in both acute antigenic responses and chronic inflammatory autoimmune responses. TCR-driven NF-κB activation up-regulates the expression of miR-146a, which in turn down-regulates NF-κB activity, at least partly through repressing the NF-κB signaling transducers TRAF6 and IRAK1. Thus, our results identify miR-146a as an important new member of the negative feedback loop that controls TCR signaling to NF-κB. Our findings also add microRNA to the list of regulators that control the resolution of T cell responses.
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Cites
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Self-citationmiR-146a modulates autoreactive Th17 cell differentiation and regulates organ-specific autoimmunity
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Noncoding RNAs regulate NF-κB signaling to modulate blood vessel inflammation
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Metadata
- Authors
- Yang, L., Boldin, M. P., Yu, Y., Liu, C. S., Ea, C.-K., Ramakrishnan, P., Taganov, K. D., Zhao, J. L., & Baltimore, D.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2012-08-13
- Volume
- 209
- Issue
- 9
- Pages
- 1655-1670
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2155605501
- Cited by
- 281
- References
- 11
- FWCI
- 9.62
- Type
- journal article
- Language
- en
- Open access
- bronze
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