TNF-α-mediated microRNA-136 induces differentiation of myeloid cells by targeting NFIA

Mei, Shiyue; Liu, Yu; Wu, Xue; He, Qingsheng; Song, Min; Li, Ling; Zhang, Yuan; Yang, Rongcun

doi:10.1189/jlb.1a0115-032rr

Cited by 13 publications

(8 citation statements)

References 38 publications

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“…Decreased expression of CD11b on monocyte subsets may stem from effective reduction of disease activity due to TNFi treatment, paralleled by a reduction in activation markers characteristic of active disease. CD11b is described as crucial in myeloid lineage differentiation, with TNF-α inhibition decreasing its expression on myeloid cells [26]. However, in RA, expression of CD11b is higher than in healthy controls and decreases after glucocorticoid treatment, which suggests that CD11b is an indicator of disease activity, rather than selectively tied to TNF-α inhibition [27].…”

Section: Discussionmentioning

confidence: 99%

TNF-α Inhibitors Decrease Classical CD14hiCD16− Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

Batko¹,

Schramm‐Luc

Skiba

et al. 2019

IJMS

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Monocytes are pivotal cells in inflammatory joint diseases. We aimed to determine the effect of TNF-α inhibitors (TNFi) on peripheral blood monocyte subpopulations and their activation in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) patients with high disease activity. To address this, we studied 50 (32 AS, 18 RA) patients with highly active disease with no prior history of TNFi use who were recruited and assigned to TNFi or placebo treatment for 12 weeks. Cytometric and clinical assessment was determined at baseline, four, and 12 weeks after initiation of TNFi treatment. We observed that treatment with TNFi led to a significant decrease in CD14hiCD16− monocytes in comparison to placebo, while circulating CD14dimCD16+ monocytes significantly increased. The TNFi-induced monocyte subset shifts were similar in RA and AS patients. While the percentage of CD14dimCD16+ monocytes increased, expression of CD11b and CD11c integrins on their surface was significantly reduced by TNFi. Additionally, CD45RA+ cells were more frequent. The shift towards nonclassical CD14dimCD16+ monocytes in peripheral blood due to TNFi treatment was seen in both AS and RA. This may reflect reduced recruitment of these cells to sites of inflammation due to lower inflammatory burden, which is associated with decreased disease activity.

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Section: Discussionmentioning

confidence: 99%

TNF-α Inhibitors Decrease Classical CD14hiCD16− Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

Batko¹,

Schramm‐Luc

Skiba

et al. 2019

IJMS

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“…These findings raise the possibility that NF‐κB might be involved in controlling Sox9 expression during the gliogenic switch in the developing cerebral cortex. A link between Nfia expression and NF‐κB was also proposed, in the context of inflammatory immune cells (Mei et al, ). Together with these earlier observations, the present findings suggest a previously uncharacterized involvement of NF‐κB in the mechanisms controlling the timing of the neurogenic‐to‐gliogenic switch in the developing cerebral cortex through the possible modulation of a number of different gene regulatory mechanisms.…”

Section: Discussionmentioning

confidence: 94%

Nuclear factor‐kappaB regulates multiple steps of gliogenesis in the developing murine cerebral cortex

Methot

Soubannier

Hermann

et al. 2018

Glia

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Nuclear factor‐kappaB (NF‐κB) is activated in neural progenitor cells in the developing murine cerebral cortex during the neurogenic phase, when it acts to prevent premature neuronal differentiation. Here we show that NF‐κB activation continues in mouse neocortical neural progenitor cells during the neurogenic‐to‐gliogenic switch. Blockade of endogenous NF‐κB activity during neocortical gliogenesis leads to the formation of supernumerary committed gliogenic progenitors and premature glial cell differentiation. Conversely, forced NF‐κB activation during the neocortical neurogenic‐to‐gliogenic transition causes delayed gliogenic commitment and decreased astroglial gene expression. NF‐κB activation continues in neocortical gliogenic progenitors following commitment and is important to inhibit the differentiation of oligodendrocyte precursor cells and to maintain persistent expression of glial fibrillary acidic protein in maturing astrocytes. These results reveal a number of previously uncharacterized roles for NF‐κB during different phases of neocortical gliogenesis and identify NF‐κB as an inhibitor of early oligodendrocyte development in the cerebral cortex.

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“…TNF-α exhibited a dual function during chronic inflammation: arresting differentiation of immature MDSCs primarily via the S100A8 and S100A9 inflammatory proteins and their corresponding receptor (RAGE) and augmenting MDSCs suppressive activity 35 . TNF-α-mediated microRNA-136 induces differentiation of myeloid cells by targeting NFIA 36 . Endogenous chronic TNF-α signaling promotes tumor growth by maintaining MDSCs survival in the transplanted tumor model 37 .…”

Section: Discussionmentioning

confidence: 99%

Mannan-Binding Lectin Deficiency Limits Inflammation-induced Myeloid-Derived Suppressor Cells Expansion via Modulating Tumor Necrosis Factor Alpha-triggered Apoptosis

Dong¹,

Jiang²,

Chen³

et al. 2022

Int. J. Biol. Sci.

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Background: Mannan-binding lectin (MBL), a soluble pattern recognition molecule in the innate immune system, is reported to be associated with the function of immune cells. Myeloid-derived suppressor cells (MDSCs) are mainly characterized by immunosuppressive activities involving several inflammatory diseases such as cancer, infection, and arthritis. Some of the factors inducing their apoptosis are known, however, mechanisms have not been identified. The underlying impact of MBL on the MDSCs especially under inflammatory conditions remains unknown. This study was designed to investigate whether MBL affects MDSCs survival during inflammation conditions. Methods: WT and MBL-deficient (MBL) mice were induced on day 0 of the experiment by subcutaneous injection of complete Freund's adjuvant and then injected with incomplete Freund's adjuvant into the knee joint space under general anesthesia on day 14 to induce inflammatory arthritis. The proportions of MDSCs in the spleen and blood and the serum level of the inflammatory cytokines were measured. In vitro study, MDSCs were isolated from the bone marrow of WT and MBL − / − mice and cultured in the presence of interleukin-6 (IL-6) and granulocyte-macrophage colony-stimulating factor (GM-CSF) for 5 days with or without tumor necrosis factor-alpha (TNF-α).Results: After adjuvant treatment, MBL − / − mice had a significantly lower frequency of MDSCs as well as elevated serum inflammatory cytokines levels compared to WT mice. MBL deficiency markedly inhibited the MDSCs frequency from mice bone marrow induced by IL-6 and GM-CSF in the presence of TNF-α in vitro. Mechanistic studies established that MBL inhibited MDSCs apoptosis via down-regulation of TNF-α/tumor necrosis factor-alpha receptor 1 (TNFR1) signaling pathway and subsequent caspase 3-dependent manner. Conclusion: Mannan-binding lectin deficiency inhibits myeloid-derived suppressor cells expansion via modulating TNF-α triggered apoptosis.

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TNF-α-mediated microRNA-136 induces differentiation of myeloid cells by targeting NFIA

Cited by 13 publications

References 38 publications

TNF-α Inhibitors Decrease Classical CD14hiCD16− Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

TNF-α Inhibitors Decrease Classical CD14hiCD16− Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

Nuclear factor‐kappaB regulates multiple steps of gliogenesis in the developing murine cerebral cortex

Mannan-Binding Lectin Deficiency Limits Inflammation-induced Myeloid-Derived Suppressor Cells Expansion via Modulating Tumor Necrosis Factor Alpha-triggered Apoptosis

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