The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
MicroRNA-148/152 Impair Innate Response and Antigen Presentation of TLR-Triggered Dendritic Cells by Targeting CaMKIIα
Abstract
MicroRNAs (miRNAs) are involved in the regulation of immunity, including the lymphocyte development and differentiation, and inflammatory cytokine production. Dendritic cells (DCs) play important roles in linking innate and adaptive immune responses. However, few miRNAs have been found to regulate the innate response and APC function of DCs to date. Calcium/calmodulin-dependent protein kinase II (CaMKII), a major downstream effector of calcium (Ca2+), has been shown to be an important regulator of the maturation and function of DCs. Our previous study showed that CaMKIIα could promote TLR-triggered production of proinflammatory cytokines and type I IFN. Inspired by the observations that dicer mutant Drosophila display defect in endogenous miRNA generation and higher CaMKII expression, we wondered whether miRNAs can regulate the innate response and APC function of DCs by targeting CaMKIIα. By predicting with software and confirming with functional experiments, we demonstrate that three members of the miRNA (miR)-148 family, miR-148a, miR-148b, and miR-152, are negative regulators of the innate response and Ag-presenting capacity of DCs. miR-148/152 expression was upregulated, whereas CaMKIIα expression was downregulated in DCs on maturation and activation induced by TLR3, TLR4, and TLR9 agonists. We showed that miR-148/152 in turn inhibited the production of cytokines including IL-12, IL-6, TNF-α, and IFN-β upregulation of MHC class II expression and DC-initiated Ag-specific T cell proliferation by targeting CaMKIIα. Therefore, miRNA-148/152 can act as fine-tuner in regulating the innate response and Ag-presenting capacity of DCs, which may contribute to the immune homeostasis and immune regulation.
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Cites
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“A single miRNA might tune protein expression from thousands of genes by direct or indirect effects (41).”
BackgroundMicroRNA-155 is induced during the macrophage inflammatory response
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Requirement of bic/microRNA-155 for Normal Immune Function
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The E3 ubiquitin ligase Nrdp1 'preferentially' promotes TLR-mediated production of type I interferon
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Cited by
Mechanism of transfer of functional microRNAs between mouse dendritic cells via exosomes.
Montecalvo, A., Larregina, A. T., Shufesky, W. J., Beer Stolz, D., Sullivan, M. L. G., Karlsson, J. M., Baty, C. J., Gibson, G. A., Erdos, G., Wang, Z., et al. (2012) · Blood · doi:10.1182/blood-2011-02-338004 · Cited by 1,429
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Bovine milk contains microRNA and messenger RNA that are stable under degradative conditions
Izumi, H., Kosaka, N., Shimizu, T., Sekine, K., Ochiya, T., & Takase, M. (2012) · Journal of Dairy Science · doi:10.3168/jds.2012-5489 · Cited by 383
Bovine milk exosomes contain microRNA and mRNA and are taken up by human macrophages
Izumi, H., Tsuda, M., Sato, Y., Kosaka, N., Ochiya, T., Iwamoto, H., Namba, K., & Takeda, Y. (2015) · Journal of Dairy Science · doi:10.3168/jds.2014-9076 · Cited by 360
Tong, L., Hao, H., Zhang, Z., Lv, Y., Liang, X., Liu, Q., Liu, T., Gong, P., Zhang, L., Cao, F., et al. (2021) · Theranostics · doi:10.7150/thno.62046 · Cited by 325
Metadata
- Authors
- Liu, X., Zhan, Z., Xu, L., Ma, F., Li, D., Guo, Z., Li, N., & Cao, X.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-12
- Volume
- 185
- Issue
- 12
- Pages
- 7244-7251
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2167875873
- Cited by
- 269
- References
- 7
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: MicroRNA-148/152 Impair Innate Response and Antigen Presentation of TLR-Triggered Dendritic Cells by Targeting CaMKIIα. https://app.cochat.ai/papers/10.4049/jimmunol.1001573
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- Liu, X., Zhan, Z., Xu, L., Ma, F., Li, D., Guo, Z., Li, N., & Cao, X. (2010). MicroRNA-148/152 Impair Innate Response and Antigen Presentation of TLR-Triggered Dendritic Cells by Targeting CaMKIIα. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1001573
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