ArticleCellular & molecular immunology2016
Activation of TLR7 increases CCND3 expression via the downregulation of miR-15b in B cells of systemic lupus erythematosus.
Article in Cellular & molecular immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- A tumor suppressor role of the miR-15b/16-2 cluster in T-cell acute lymphoblastic leukemia.Blood · 2026Article
- CD21 primes extrafollicular differentiation of autoreactive B cells in a TLR7-driven lupus model.Science immunology · 2025Article
- RNA NExperimental & molecular medicine · 2025Article
- Nicotinamide boosts oocyte quantity and quality by promoting N4-acetylation modification in lupus mice.Science advances · 2025Article
- Role of miRNAs in Apoptosis Pathways of Immune Cells in Systemic Lupus Erythematosus.Immunity, inflammation and disease · 2025Review
- High expression of GPR50 promotes the proliferation, migration and autophagy of hepatocellular carcinoma cells in vitro.Journal of cell communication and signaling · 2023Article
- Dysregulated MicroRNAs in the Pathogenesis of Systemic Lupus Erythematosus: A Comprehensive Review.International journal of biological sciences · 2023Review
- Deficiency of p53 Causes the Inadequate Expression of miR-1246 in B Cells of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- An update on epigenetic regulation in autoimmune diseases.Journal of translational autoimmunity · 2022Article
- MicroRNAs in Lupus Nephritis-Role in Disease Pathogenesis and Clinical Applications.International journal of molecular sciences · 2021Review
- Escape from X chromosome inactivation and female bias of autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2020Review
- miR-138-5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3.Oncology letters · 2020Article
- Excessive miR-152-3p Results in Increased BAFF Expression in SLE B-Cells by Inhibiting the KLF5 Expression.Frontiers in immunology · 2019Article
- Pim-3 enhances melanoma cell migration and invasion by promoting STAT3 phosphorylation.Cancer biology & therapy · 2018Article
- TLR7, a third signal for the robust generation of spontaneous germinal center B cells in systemic lupus erythematosus.Cellular & molecular immunology · 2018Article
- B Cell-Related Circulating MicroRNAs With the Potential Value of Biomarkers in the Differential Diagnosis, and Distinguishment Between the Disease Activity and Lupus Nephritis for Systemic Lupus Erythematosus.Frontiers in immunology · 2018Article
- The Involvement of MicroRNAs in Modulation of Innate and Adaptive Immunity in Systemic Lupus Erythematosus and Lupus Nephritis.Journal of immunology research · 2018Review
- Ligation of CD180 inhibits IFN-α signaling in a Lyn-PI3K-BTK-dependent manner in B cells.Cellular & molecular immunology · 2017Article
- miR-15a-3p and miR-16-1-3p Negatively Regulate Twist1 to Repress Gastric Cancer Cell Invasion and Metastasis.International journal of biological sciences · 2017Article
- Notch-Hes-1 axis controls TLR7-mediated autophagic death of macrophage via induction of P62 in mice with lupus.Cell death & disease · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by B-cell hyperreactivity. The Toll-like receptor 7 (TLR7) signaling pathway is abnormally activated in SLE B cells. CyclinD3 (CCND3) plays an important role in B-cell proliferation, development, and differentiation. Although previous studies focused on the B cell-intrinsic role of TLR7 for the development of spontaneous germinal centers, the influence of TLR7 on CCND3 in SLE B cells is still not clear. Here, we used a B-cell profiling chip and found that CCND3 was related to SLE and significantly elevated in SLE B cells. Moreover, we determined that the expression level of CCND3 was higher, while miR-15b was significantly lower in the B cells from SLE patients and B6.MRL-Faslpr/J lupus mice compared to normal subjects. Furthermore, we demonstrated that the activation of TLR7 dramatically increased CCND3 expression but significantly decreased miR-15b in B cells in vitro and we identified that CCND3 is a direct target of miR-15b. To further confirm our results, we established another lupus model by topically treating C57BL/6 (B6) mice with the TLR-7 agonist imiquimod (IMQ) for 8 weeks according to the previously described protocol. Expectedly, topical treatment with IMQ also significantly increased CCND3 and decreased miR-15b in B cells of B6 mice. Taken together, our results identified that the activation of TLR7 increased CCND3 expression via the downregulation of miR-15b in B cells; thus, these findings suggest that extrinsic factor-induced CCND3 expression may contribute to the abnormality of B cell in SLE.
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